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José Pedraza-Chaverri
Facultad de Química, Departamento de Biología, Universidad Nacional Autónoma de México, CDMX 04510, Mexico

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Review
Published: 24 August 2021 in Biomolecules
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Mitochondria are complex organelles that orchestrate several functions in the cell. The primary function recognized is energy production; however, other functions involve the communication with the rest of the cell through reactive oxygen species (ROS), calcium influx, mitochondrial DNA (mtDNA), adenosine triphosphate (ATP) levels, cytochrome c release, and also through tricarboxylic acid (TCA) metabolites. Kidney function highly depends on mitochondria; hence mitochondrial dysfunction is associated with kidney diseases. In addition to oxidative phosphorylation impairment, other mitochondrial abnormalities have been described in kidney diseases, such as induction of mitophagy, intrinsic pathway of apoptosis, and releasing molecules to communicate to the rest of the cell. The TCA cycle is a metabolic pathway whose primary function is to generate electrons to feed the electron transport system (ETS) to drives energy production. However, TCA cycle metabolites can also release from mitochondria or produced in the cytosol to exert different functions and modify cell behavior. Here we review the involvement of some of the functions of TCA metabolites in kidney diseases.

ACS Style

Alexis Paulina Jiménez-Uribe; Estefani Yaquelin Hernández-Cruz; Karla Jaqueline Ramírez-Magaña; José Pedraza-Chaverri. Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases. Biomolecules 2021, 11, 1259 .

AMA Style

Alexis Paulina Jiménez-Uribe, Estefani Yaquelin Hernández-Cruz, Karla Jaqueline Ramírez-Magaña, José Pedraza-Chaverri. Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases. Biomolecules. 2021; 11 (9):1259.

Chicago/Turabian Style

Alexis Paulina Jiménez-Uribe; Estefani Yaquelin Hernández-Cruz; Karla Jaqueline Ramírez-Magaña; José Pedraza-Chaverri. 2021. "Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases." Biomolecules 11, no. 9: 1259.

Review article
Published: 24 August 2021 in Cellular Signalling
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The fibrotic process could be easily defined as a pathological excess of extracellular matrix deposition, leading to disruption of tissue architecture and eventually loss of function; however, this process involves a complex network of several signal transduction pathways. Virtually almost all organs could be affected by fibrosis, the most affected are the liver, lung, skin, kidney, heart, and eyes; in all of them, the transforming growth factor-beta (TGF-β) has a central role. The canonical and non-canonical signal pathways of TGF-β impact the fibrotic process at the cellular and molecular levels, inducing the epithelial-mesenchymal transition (EMT) and the induction of profibrotic gene expression with the consequent increase in proteins such as alpha-smooth actin (α-SMA), fibronectin, collagen, and other extracellular matrix proteins. Recently, it has been reported that some molecules that have not been typically associated with the fibrotic process, such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4), mammalian target of rapamycin (mTOR), histone deacetylases (HDAC), and sphingosine-1 phosphate (S1P); are critical in its development. In this review, we describe and discuss the role of these new players of fibrosis and the convergence with TGF-β signaling pathways, unveiling new insights into the panorama of fibrosis that could be useful for future therapeutic targets.

ACS Style

Alexis Paulina Jiménez-Uribe; Tania Gómez-Sierra; Omar Emiliano Aparicio-Trejo; Marisol Orozco-Ibarra; José Pedraza-Chaverri. Backstage players of fibrosis: NOX4, mTOR, HDAC, and S1P; companions of TGF-β. Cellular Signalling 2021, 87, 110123 .

AMA Style

Alexis Paulina Jiménez-Uribe, Tania Gómez-Sierra, Omar Emiliano Aparicio-Trejo, Marisol Orozco-Ibarra, José Pedraza-Chaverri. Backstage players of fibrosis: NOX4, mTOR, HDAC, and S1P; companions of TGF-β. Cellular Signalling. 2021; 87 ():110123.

Chicago/Turabian Style

Alexis Paulina Jiménez-Uribe; Tania Gómez-Sierra; Omar Emiliano Aparicio-Trejo; Marisol Orozco-Ibarra; José Pedraza-Chaverri. 2021. "Backstage players of fibrosis: NOX4, mTOR, HDAC, and S1P; companions of TGF-β." Cellular Signalling 87, no. : 110123.

Review
Published: 03 August 2021 in Biomolecules
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Mitochondria are essential organelles in physiology and kidney diseases, because they produce cellular energy required to perform their function. During mitochondrial metabolism, reactive oxygen species (ROS) are produced. ROS function as secondary messengers, inducing redox-sensitive post-translational modifications (PTM) in proteins and activating or deactivating different cell signaling pathways. However, in kidney diseases, ROS overproduction causes oxidative stress (OS), inducing mitochondrial dysfunction and altering its metabolism and dynamics. The latter processes are closely related to changes in the cell redox-sensitive signaling pathways, causing inflammation and apoptosis cell death. Although mitochondrial metabolism, ROS production, and OS have been studied in kidney diseases, the role of redox signaling pathways in mitochondria has not been addressed. This review focuses on altering the metabolism and dynamics of mitochondria through the dysregulation of redox-sensitive signaling pathways in kidney diseases.

ACS Style

Ana Aranda-Rivera; Alfredo Cruz-Gregorio; Omar Aparicio-Trejo; José Pedraza-Chaverri. Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases. Biomolecules 2021, 11, 1144 .

AMA Style

Ana Aranda-Rivera, Alfredo Cruz-Gregorio, Omar Aparicio-Trejo, José Pedraza-Chaverri. Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases. Biomolecules. 2021; 11 (8):1144.

Chicago/Turabian Style

Ana Aranda-Rivera; Alfredo Cruz-Gregorio; Omar Aparicio-Trejo; José Pedraza-Chaverri. 2021. "Mitochondrial Redox Signaling and Oxidative Stress in Kidney Diseases." Biomolecules 11, no. 8: 1144.

Journal article
Published: 23 July 2021 in International Journal of Molecular Sciences
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Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by increased activation of fibroblasts/myofibroblasts. Previous reports have shown that IPF fibroblasts are resistant to apoptosis, but the mechanisms remain unclear. Since inhibition of the mitochondrial permeability transition pore (mPTP) has been implicated in the resistance to apoptosis, in this study, we analyzed the role of mitochondrial function and the mPTP on the apoptosis resistance of IPF fibroblasts under basal conditions and after mitomycin C-induced apoptosis. We measured the release of cytochrome c, mPTP opening, mitochondrial calcium release, oxygen consumption, mitochondrial membrane potential, ADP/ATP ratio, ATP concentration, and mitochondrial morphology. We found that IPF fibroblasts were resistant to mitomycin C-induced apoptosis and that calcium, a well-established activator of mPTP, is decreased as well as the release of pro-apoptotic proteins such as cytochrome c. Likewise, IPF fibroblasts showed decreased mitochondrial function, while mPTP was less sensitive to ionomycin-induced opening. Although IPF fibroblasts did not present changes in the mitochondrial membrane potential, we found a fragmented mitochondrial network with scarce, thinned, and disordered mitochondria with reduced ATP levels. Our findings demonstrate that IPF fibroblasts are resistant to mitomycin C-induced apoptosis and that altered mPTP opening contributes to this resistance. In addition, IPF fibroblasts show mitochondrial dysfunction evidenced by a decrease in respiratory parameters.

ACS Style

Erika Luis-García; Carina Becerril; Alfonso Salgado-Aguayo; Omar Aparicio-Trejo; Yair Romero; Edgar Flores-Soto; Criselda Mendoza-Milla; Martha Montaño; Victoria Chagoya; José Pedraza-Chaverri; Mohammed El Hafidi; Marisol Orozco-Ibarra; Annie Pardo; Moisés Selman. Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts. International Journal of Molecular Sciences 2021, 22, 7870 .

AMA Style

Erika Luis-García, Carina Becerril, Alfonso Salgado-Aguayo, Omar Aparicio-Trejo, Yair Romero, Edgar Flores-Soto, Criselda Mendoza-Milla, Martha Montaño, Victoria Chagoya, José Pedraza-Chaverri, Mohammed El Hafidi, Marisol Orozco-Ibarra, Annie Pardo, Moisés Selman. Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts. International Journal of Molecular Sciences. 2021; 22 (15):7870.

Chicago/Turabian Style

Erika Luis-García; Carina Becerril; Alfonso Salgado-Aguayo; Omar Aparicio-Trejo; Yair Romero; Edgar Flores-Soto; Criselda Mendoza-Milla; Martha Montaño; Victoria Chagoya; José Pedraza-Chaverri; Mohammed El Hafidi; Marisol Orozco-Ibarra; Annie Pardo; Moisés Selman. 2021. "Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts." International Journal of Molecular Sciences 22, no. 15: 7870.

Journal article
Published: 16 July 2021 in Biology
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Our work evaluated cardiac function and mitochondrial bioenergetics parameters in hearts from male Wistar rats subjected to the UUO model during 28 days of progression. We measured markers of kidney damage and inflammation in plasma and renal fibrosis by histological analysis and Western blot. Cardiac function was evaluated by echocardiography and proteins involved in cardiac damage by Western blot. Oxygen consumption and transmembrane potential were monitored in cardiac mitochondria using high-resolution respirometry. We also determined the activity of ATP synthase and antioxidant enzymes such as glutathione peroxidase, glutathione reductase, and catalase. Our results show that, although renal dysfunction is established in animals subjected to ureteral obstruction, cardiac function is maintained along with mitochondrial function and antioxidant enzymes activity after 28 days of injury evolution. Our results suggest that renocardiac syndrome might develop but belatedly in obstruction-induced renal damage, opening the opportunity for treatment to prevent this condition.

ACS Style

Rodrigo Prieto-Carrasco; Alejandro Silva-Palacios; Pedro Rojas-Morales; Omar Aparicio-Trejo; Estefany Medina-Reyes; Estefani Hernández-Cruz; Carlos Sánchez-Garibay; Citlaltepetl Salinas-Lara; Natalia Pavón; Francisco Roldán; Cecilia Zazueta; Edilia Tapia; José Pedraza-Chaverri. Unilateral Ureteral Obstruction for 28 Days in Rats Is Not Associated with Changes in Cardiac Function or Alterations in Mitochondrial Function. Biology 2021, 10, 671 .

AMA Style

Rodrigo Prieto-Carrasco, Alejandro Silva-Palacios, Pedro Rojas-Morales, Omar Aparicio-Trejo, Estefany Medina-Reyes, Estefani Hernández-Cruz, Carlos Sánchez-Garibay, Citlaltepetl Salinas-Lara, Natalia Pavón, Francisco Roldán, Cecilia Zazueta, Edilia Tapia, José Pedraza-Chaverri. Unilateral Ureteral Obstruction for 28 Days in Rats Is Not Associated with Changes in Cardiac Function or Alterations in Mitochondrial Function. Biology. 2021; 10 (7):671.

Chicago/Turabian Style

Rodrigo Prieto-Carrasco; Alejandro Silva-Palacios; Pedro Rojas-Morales; Omar Aparicio-Trejo; Estefany Medina-Reyes; Estefani Hernández-Cruz; Carlos Sánchez-Garibay; Citlaltepetl Salinas-Lara; Natalia Pavón; Francisco Roldán; Cecilia Zazueta; Edilia Tapia; José Pedraza-Chaverri. 2021. "Unilateral Ureteral Obstruction for 28 Days in Rats Is Not Associated with Changes in Cardiac Function or Alterations in Mitochondrial Function." Biology 10, no. 7: 671.

Journal article
Published: 24 June 2021 in Free Radical Biology and Medicine
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Renal fibrosis is a well-known mechanism that favors chronic kidney disease (CKD) development in obstructive nephropathy, a significant pathology worldwide. Fibrosis induction involves several pathways, and although mitochondrial alterations have recently emerged as a critical factor that triggers renal damage in the obstructed kidney, the temporal mitochondrial alterations during the fibrotic induction remain unexplored. Therefore, in this work, we evaluated the time course of mitochondrial mass and bioenergetics alterations induced by a unilateral ureteral obstruction (UUO), a widely used model to study the mechanism involved in kidney fibrosis induction and progression. Our results show a marked reduction in mitochondrial oxidative phosphorylation (OXPHOS) in the obstructed kidney on days 7 to 28 of obstruction without significant mitochondrial coupling changes. Besides, we observed that mitochondrial mass was reduced, probably due to decreased biogenesis and mitophagy induction. OXPHOS impairment was associated with decreased mitochondrial biogenesis markers, the peroxisome proliferator-activated receptor γ co-activator-1alpha (PGC-1α), and nuclear respiratory factor 1 (NRF1); and also, with the induction of mitophagy in a PTEN-induced kinase 1 (PINK1) and Parkin independent way. It is concluded that the impairment of OXPHOS capacity may be explained by the reduction in mitochondrial biogenesis and the induction of mitophagy during fibrotic progression.

ACS Style

Alexis Paulina Jiménez-Uribe; Belen Bellido; Omar Emiliano Aparicio-Trejo; Edilia Tapia; Laura Gabriela Sánchez-Lozada; José Antonio Hernández-Santos; Francisca Fernández-Valverde; Estefani Yaquelin Hernández-Cruz; Marisol Orozco-Ibarra; José Pedraza-Chaverri. Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats. Free Radical Biology and Medicine 2021, 172, 358 -371.

AMA Style

Alexis Paulina Jiménez-Uribe, Belen Bellido, Omar Emiliano Aparicio-Trejo, Edilia Tapia, Laura Gabriela Sánchez-Lozada, José Antonio Hernández-Santos, Francisca Fernández-Valverde, Estefani Yaquelin Hernández-Cruz, Marisol Orozco-Ibarra, José Pedraza-Chaverri. Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats. Free Radical Biology and Medicine. 2021; 172 ():358-371.

Chicago/Turabian Style

Alexis Paulina Jiménez-Uribe; Belen Bellido; Omar Emiliano Aparicio-Trejo; Edilia Tapia; Laura Gabriela Sánchez-Lozada; José Antonio Hernández-Santos; Francisca Fernández-Valverde; Estefani Yaquelin Hernández-Cruz; Marisol Orozco-Ibarra; José Pedraza-Chaverri. 2021. "Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats." Free Radical Biology and Medicine 172, no. : 358-371.

Review
Published: 17 June 2021 in Antioxidants
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Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.

ACS Style

Noemí Cárdenas-Rodríguez; Cindy Bandala; América Vanoye-Carlo; Iván Ignacio-Mejía; Saúl Gómez-Manzo; Estefani Hernández-Cruz; José Pedraza-Chaverri; Liliana Carmona-Aparicio; Beatriz Hernández-Ochoa. Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19. Antioxidants 2021, 10, 971 .

AMA Style

Noemí Cárdenas-Rodríguez, Cindy Bandala, América Vanoye-Carlo, Iván Ignacio-Mejía, Saúl Gómez-Manzo, Estefani Hernández-Cruz, José Pedraza-Chaverri, Liliana Carmona-Aparicio, Beatriz Hernández-Ochoa. Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19. Antioxidants. 2021; 10 (6):971.

Chicago/Turabian Style

Noemí Cárdenas-Rodríguez; Cindy Bandala; América Vanoye-Carlo; Iván Ignacio-Mejía; Saúl Gómez-Manzo; Estefani Hernández-Cruz; José Pedraza-Chaverri; Liliana Carmona-Aparicio; Beatriz Hernández-Ochoa. 2021. "Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19." Antioxidants 10, no. 6: 971.

Review article
Published: 12 June 2021 in Free Radical Biology and Medicine
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High-risk human papillomavirus (HR-HPVs) are associated with the development of cervical, anus, vagina, vulva, penis, and oropharynx cancer. HR-HPVs target and modify the function of different cell biomolecules such as glucose, amino acids, lipids, among others. The latter induce cell proliferation, cell death evasion, and genomic instability resulting in cell transformation. Moreover, lipids are essential biomolecules in HR-HPVs infection and cell vesicular trafficking. They are also critical in producing cellular energy, the epithelial-mesenchymal transition (EMT) process, and therapy resistance of HPV-related cancers. HPV proteins induce oxidative stress (OS), which in turn promotes lipid peroxidation and cell damage, resulting in cell death such as apoptosis, autophagy, and ferroptosis. HR-HPV-related cancer cells cope with OS and lipid peroxidation, preventing cell death; however, these cells are sensitized by OS, which could be used as a target for redox therapies to induce their elimination. This review focuses on the role of lipids in HR-HPV infection and HPV-related cancer development, maintenance, resistance to therapy, and the possible treatments associated with lipids. Furthermore, we emphasize the significant role of OS in lipid peroxidation to induce cell death through apoptosis, autophagy, and ferroptosis to eliminate HPV-related cancers.

ACS Style

Alfredo Cruz-Gregorio; Ana Karina Aranda-Rivera; Ariadna Jazmin Ortega-Lozano; José Pedraza Chaverri; Francisco Mendoza Hoffmann. Lipid Metabolism and Oxidative Stress in HPV-related cancers. Free Radical Biology and Medicine 2021, 172, 226 -236.

AMA Style

Alfredo Cruz-Gregorio, Ana Karina Aranda-Rivera, Ariadna Jazmin Ortega-Lozano, José Pedraza Chaverri, Francisco Mendoza Hoffmann. Lipid Metabolism and Oxidative Stress in HPV-related cancers. Free Radical Biology and Medicine. 2021; 172 ():226-236.

Chicago/Turabian Style

Alfredo Cruz-Gregorio; Ana Karina Aranda-Rivera; Ariadna Jazmin Ortega-Lozano; José Pedraza Chaverri; Francisco Mendoza Hoffmann. 2021. "Lipid Metabolism and Oxidative Stress in HPV-related cancers." Free Radical Biology and Medicine 172, no. : 226-236.

Journal article
Published: 04 June 2021 in Toxics
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The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that heterodimerizes with the AhR nuclear translocator (ARNT) to modulate CYP1A1 expression, a gene involved in the biotransformation of benzo[a]pyrene (BaP). The AhR pathway shows daily variations under the control of the circadian timing system. Daytime restricted feeding (DRF) entrains the expression of genes involved in the processing of nutrients and xenobiotics to food availability. Therefore, we evaluate if temporal AhR, ARNT, and CYP1A1 hepatic expression in rats are due to light/dark cycles or fasting/feeding cycles promoted by DRF. Our results show that AhR oscillates throughout the 24 h period in DRF and ad libitum feeding rats (ALF), showing maximum expression at the same time points. DRF modified the peak of ARNT expression at ZT5; meanwhile, ALF animals showed a peak of maximum expression at ZT17. An increased expression of CYP1A1 was linked to the meal time in both groups of animals. Although a high CYP1A1 expression has been previously associated with BaP genotoxicity, our results show that, compared with the ALF group, DRF attenuated the BaP-CYP1A1 induction potency, the liver DNA-BaP adducts, the liver concentration of unmetabolized BaP, and the blood aspartate aminotransferase and alanine aminotransferase activities when BaP is administered prior to the acrophase of CYP1A1 expression. These results demonstrate that DRF modifies the ARNT and CYP1A1 expression and protects from BaP toxicity.

ACS Style

Oscar Ávila-Rosales; Mauricio Díaz-Muñoz; Rafael Camacho-Carranza; Elvia Coballase-Urrutia; José Pedraza-Chaverri; Jorge García-Rebollar; Jesús Espinosa-Aguirre. Daytime Restricted Feeding Modifies the Temporal Expression of CYP1A1 and Attenuated Damage Induced by Benzo[a]pyrene in Rat Liver When Administered before CYP1A1 Acrophase. Toxics 2021, 9, 130 .

AMA Style

Oscar Ávila-Rosales, Mauricio Díaz-Muñoz, Rafael Camacho-Carranza, Elvia Coballase-Urrutia, José Pedraza-Chaverri, Jorge García-Rebollar, Jesús Espinosa-Aguirre. Daytime Restricted Feeding Modifies the Temporal Expression of CYP1A1 and Attenuated Damage Induced by Benzo[a]pyrene in Rat Liver When Administered before CYP1A1 Acrophase. Toxics. 2021; 9 (6):130.

Chicago/Turabian Style

Oscar Ávila-Rosales; Mauricio Díaz-Muñoz; Rafael Camacho-Carranza; Elvia Coballase-Urrutia; José Pedraza-Chaverri; Jorge García-Rebollar; Jesús Espinosa-Aguirre. 2021. "Daytime Restricted Feeding Modifies the Temporal Expression of CYP1A1 and Attenuated Damage Induced by Benzo[a]pyrene in Rat Liver When Administered before CYP1A1 Acrophase." Toxics 9, no. 6: 130.

Review article
Published: 30 May 2021 in Free Radical Biology and Medicine
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Unilateral ureteral obstruction (UUO) is an experimental rodent model that mimics renal fibrosis associated with obstructive nephropathy in an accelerated manner. After UUO, the activation of the renin-angiotensin system (RAS), nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and mitochondrial dysfunction lead to reactive oxygen species (ROS) overproduction in the kidney. ROS are secondary messengers able to induce post-translational modifications (PTMs) in redox-sensitive proteins, which activate or deactivate signaling pathways. Therefore, in UUO, it has been proposed that ROS overproduction causes changes in said pathways promoting inflammation, oxidative stress, and apoptosis that contribute to fibrosis development. Furthermore, mitochondrial metabolism impairment has been associated with UUO, contributing to renal damage in this model. Although ROS production and oxidative stress have been studied in UUO, the development of renal fibrosis associated with redox signaling pathways has not been addressed. This review focuses on the current information about the activation and deactivation of signaling pathways sensitive to a redox state and their effect on mitochondrial metabolism in the fibrosis development in the UUO model.

ACS Style

Ana Karina Aranda-Rivera; Alfredo Cruz-Gregorio; Omar Emiliano Aparicio-Trejo; Ariadna Jazmín Ortega-Lozano; José Pedraza-Chaverri. Redox signaling pathways in unilateral ureteral obstruction (UUO)-induced renal fibrosis. Free Radical Biology and Medicine 2021, 172, 65 -81.

AMA Style

Ana Karina Aranda-Rivera, Alfredo Cruz-Gregorio, Omar Emiliano Aparicio-Trejo, Ariadna Jazmín Ortega-Lozano, José Pedraza-Chaverri. Redox signaling pathways in unilateral ureteral obstruction (UUO)-induced renal fibrosis. Free Radical Biology and Medicine. 2021; 172 ():65-81.

Chicago/Turabian Style

Ana Karina Aranda-Rivera; Alfredo Cruz-Gregorio; Omar Emiliano Aparicio-Trejo; Ariadna Jazmín Ortega-Lozano; José Pedraza-Chaverri. 2021. "Redox signaling pathways in unilateral ureteral obstruction (UUO)-induced renal fibrosis." Free Radical Biology and Medicine 172, no. : 65-81.

Review article
Published: 27 May 2021 in Advances in Redox Research
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Endoplasmic reticulum (ER) stress is induced by intrinsic and extrinsic factors and, in consequence, activates the unfolded protein response (UPR); which in an acute phase restores cellular homeostasis, whereas in a chronic phase promotes apoptosis. ER stress has been detected in a broad range of kidney diseases and the different degrees of ER stress and UPR stimulation could activate antioxidant and immune responses, autophagy, cell maintenance, inflammation, apoptosis and fibrosis. Understanding the regulation of ER stress and the UPR signaling pathways will allow to develop treatments that favor cellular functions in order to reduce the progression of diseases. The regulation of ER stress is carried out with natural or pharmacological compounds. The pharmacological inhibitors of ER stress commonly used are 4-phenylbutyric acid (4-PBA), tauroursodeoxycholic acid (TUDCA) and salubrinal, whereas pharmacological inducers of ER stress generally used are thapsigargin and tunicamycin. In addition, natural compounds such as polyphenols are able to induce and inhibit ER stress, and their effects are dose-dependent. In this review, we summarize notable findings on strategies of the induction of ER stress, as well as its inhibition, in the context of kidney diseases. Furthermore, these two methods of regulating ER stress are discussed.

ACS Style

Tania Gómez-Sierra; Belen Bellido; Laura María Reyes-Fermín; Elena Martínez-Klimova; José Pedraza-Chaverri. Regulation of endoplasmic reticulum stress in models of kidney disease. Advances in Redox Research 2021, 3, 100010 .

AMA Style

Tania Gómez-Sierra, Belen Bellido, Laura María Reyes-Fermín, Elena Martínez-Klimova, José Pedraza-Chaverri. Regulation of endoplasmic reticulum stress in models of kidney disease. Advances in Redox Research. 2021; 3 ():100010.

Chicago/Turabian Style

Tania Gómez-Sierra; Belen Bellido; Laura María Reyes-Fermín; Elena Martínez-Klimova; José Pedraza-Chaverri. 2021. "Regulation of endoplasmic reticulum stress in models of kidney disease." Advances in Redox Research 3, no. : 100010.

Journal article
Published: 21 April 2021 in Biology
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The five-sixth nephrectomy (5/6Nx) model is widely used to study the mechanisms involved in chronic kidney disease (CKD) progression. Mitochondrial impairment is a critical mechanism that favors CKD progression. However, until now, there are no temporal studies of the change in mitochondrial biogenesis and dynamics that allow determining the role of these processes in mitochondrial impairment and renal damage progression in the 5/6Nx model. In this work, we determined the changes in mitochondrial biogenesis and dynamics markers in remnant renal mass from days 2 to 28 after 5/6Nx. Our results show a progressive reduction in mitochondrial biogenesis triggered by reducing two principal regulators of mitochondrial protein expression, the peroxisome proliferator-activated receptor-gamma coactivator 1-alpha and the peroxisome proliferator-activated receptor alpha. Furthermore, the reduction in mitochondrial biogenesis proteins strongly correlates with the increase in renal damage markers. Additionally, we found a slow and gradual change in mitochondrial dynamics from fusion to fission, favoring mitochondrial fragmentation at later stages after 5/6Nx. Together, our results suggest that 5/6Nx induces the progressive reduction in mitochondrial mass over time via the decrease in mitochondrial biogenesis factors and a slow shift from mitochondrial fission to fusion; both mechanisms favor CKD progression in the remnant renal mass.

ACS Style

Rodrigo Prieto-Carrasco; Fernando García-Arroyo; Omar Aparicio-Trejo; Pedro Rojas-Morales; Juan León-Contreras; Rogelio Hernández-Pando; Laura Sánchez-Lozada; Edilia Tapia; José Pedraza-Chaverri. Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy. Biology 2021, 10, 349 .

AMA Style

Rodrigo Prieto-Carrasco, Fernando García-Arroyo, Omar Aparicio-Trejo, Pedro Rojas-Morales, Juan León-Contreras, Rogelio Hernández-Pando, Laura Sánchez-Lozada, Edilia Tapia, José Pedraza-Chaverri. Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy. Biology. 2021; 10 (5):349.

Chicago/Turabian Style

Rodrigo Prieto-Carrasco; Fernando García-Arroyo; Omar Aparicio-Trejo; Pedro Rojas-Morales; Juan León-Contreras; Rogelio Hernández-Pando; Laura Sánchez-Lozada; Edilia Tapia; José Pedraza-Chaverri. 2021. "Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy." Biology 10, no. 5: 349.

Journal article
Published: 28 February 2021 in International Journal of Molecular Sciences
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Excessive intake of fructose results in metabolic syndrome (MS) and kidney damage, partly mediated by its metabolism by fructokinase-C or ketohexokinase-C (KHK-C). Osthol has antioxidant properties, is capable of regulating adipogenesis, and inhibits KHK-C activity. Here, we examined the potential protective role of osthol in the development of kidney disease induced by a Western (high-fat/high-sugar) diet. Control rats fed with a high-fat/high-sugar diet were compared with two groups that also received two different doses of osthol (30 mg/kg/d or 40 mg/kg/d body weight BW). A fourth group served as a normal control and received regular chow. At the end of the follow-up, kidney function, metabolic markers, oxidative stress, and lipogenic enzymes were evaluated. The Western diet induced MS (hypertension, hyperglycemia, hypertriglyceridemia, obesity, hyperuricemia), a fall in the glomerular filtration rate, renal tubular damage, and increased oxidative stress in the kidney cortex, with increased expression of lipogenic enzymes and increased kidney KHK expression. Osthol treatment prevented the development of MS and ameliorated kidney damage by inhibiting KHK activity, preventing oxidative stress via nuclear factor erythroid 2-related factor (Nrf2) activation, and reducing renal lipotoxicity. These data suggest that the nutraceutical osthol might be an ancillary therapy to slow the progression of MS and kidney damage induced by a Western diet.

ACS Style

Fernando García-Arroyo; Guillermo Gonzaga-Sánchez; Edilia Tapia; Itzel Muñoz-Jiménez; Lino Manterola-Romero; Horacio Osorio-Alonso; Abraham Arellano-Buendía; José Pedraza-Chaverri; Carlos Roncal-Jiménez; Miguel Lanaspa; Richard Johnson; Laura Sánchez-Lozada. Osthol Ameliorates Kidney Damage and Metabolic Syndrome Induced by a High-Fat/High-Sugar Diet. International Journal of Molecular Sciences 2021, 22, 2431 .

AMA Style

Fernando García-Arroyo, Guillermo Gonzaga-Sánchez, Edilia Tapia, Itzel Muñoz-Jiménez, Lino Manterola-Romero, Horacio Osorio-Alonso, Abraham Arellano-Buendía, José Pedraza-Chaverri, Carlos Roncal-Jiménez, Miguel Lanaspa, Richard Johnson, Laura Sánchez-Lozada. Osthol Ameliorates Kidney Damage and Metabolic Syndrome Induced by a High-Fat/High-Sugar Diet. International Journal of Molecular Sciences. 2021; 22 (5):2431.

Chicago/Turabian Style

Fernando García-Arroyo; Guillermo Gonzaga-Sánchez; Edilia Tapia; Itzel Muñoz-Jiménez; Lino Manterola-Romero; Horacio Osorio-Alonso; Abraham Arellano-Buendía; José Pedraza-Chaverri; Carlos Roncal-Jiménez; Miguel Lanaspa; Richard Johnson; Laura Sánchez-Lozada. 2021. "Osthol Ameliorates Kidney Damage and Metabolic Syndrome Induced by a High-Fat/High-Sugar Diet." International Journal of Molecular Sciences 22, no. 5: 2431.

Review
Published: 03 February 2021 in Antioxidants
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Nutrition plays a fundamental role in the prevention and treatment of dyslipidemias and its oxidative-related complications. Currently, there is evidence about the beneficial effects of isolated antioxidants or foods enriched or added with antioxidant compounds. However, the application of the natural foods is more integrated than the analysis of a single nutrient. Our aim is compiling scientific literature regarding the nutritional strategies by foods with antioxidant effect in blood lipids, enzymatic and non-enzymatic antioxidants, and oxidative and inflammatory markers of subjects with dyslipidemia. We searched in MEDLINE/PubMed, Scopus, and Web of Science. From a total of 263 studies screened, 16 were included. Dietary strategies included walnuts, olive oil, raw almonds, G. paraguayase, white sesame, mate tea, Brazil nut flour, red wine, granulated Brazil nuts, grapes, wolfberry fruit, fermented beverage, coffee, orange, and blackberry juices showed significant differences in blood lipids, antioxidant activity, antioxidant enzymes, and oxidative and inflammatory markers. This systematic review compiling scientific studies about dietary strategies using foods with antioxidant effect to improve the antioxidant status in dyslipidemias.

ACS Style

Isabel Medina-Vera; Lizzette Gómez-De-Regil; Ana Gutiérrez-Solis; Roberto Lugo; Martha Guevara-Cruz; José Pedraza-Chaverri; Azalia Avila-Nava. Dietary Strategies by Foods with Antioxidant Effect on Nutritional Management of Dyslipidemias: A Systematic Review. Antioxidants 2021, 10, 225 .

AMA Style

Isabel Medina-Vera, Lizzette Gómez-De-Regil, Ana Gutiérrez-Solis, Roberto Lugo, Martha Guevara-Cruz, José Pedraza-Chaverri, Azalia Avila-Nava. Dietary Strategies by Foods with Antioxidant Effect on Nutritional Management of Dyslipidemias: A Systematic Review. Antioxidants. 2021; 10 (2):225.

Chicago/Turabian Style

Isabel Medina-Vera; Lizzette Gómez-De-Regil; Ana Gutiérrez-Solis; Roberto Lugo; Martha Guevara-Cruz; José Pedraza-Chaverri; Azalia Avila-Nava. 2021. "Dietary Strategies by Foods with Antioxidant Effect on Nutritional Management of Dyslipidemias: A Systematic Review." Antioxidants 10, no. 2: 225.

Review
Published: 07 January 2021 in Antioxidants
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Resveratrol (RV) is a polyphenolic compound with antioxidant, anti-inflammatory, and hypoglycemic properties. Several in vitro and animal model studies have demonstrated the beneficial effects of RV; however, the results in humans are not conclusive. After a search of different databases, 32 studies were selected for this systematic review and 30 were included in the meta-analysis. Studies that evaluated the effect of RV on glucose, insulin, HbA1c, and insulin resistance (HOMA-IR) levels were included. A significant decrease of glucose (−5.24 mg/dL, p = 0.002) and insulin levels (−1.23 mIU/L, p = 0.0003) was observed. HbA1c and HOMA-IR did not show significant changes. Due to heterogeneity, sub-analyzes were performed. Sub-analysis by dose revealed that glucose levels improve significantly after the administration of 500–1000 mg/day of RV (−7.54 mg/dL, p = 0.002), while insulin improves with doses lower than 500 mg/day (−1.43 mIU/L, p = 0.01) and greater than 1000 mg/day (−2.12 mIU/L, p = 0.03). HbA1c and HOMA-IR remained unchanged after sub-analysis by dose. Our findings suggest that RV improves glucose and insulin levels in subjects with type 2 diabetes mellitus (T2DM) and aged 45–59 years, regardless of the duration of the intervention. HbA1c improves with interventions ≥3 months. HOMA-IR does not exhibit significant changes after RV administration.

ACS Style

Beatriz Isabel García-Martínez; Mirna Ruiz-Ramos; José Pedraza-Chaverri; Edelmiro Santiago-Osorio; Víctor Manuel Mendoza-Núñez. Hypoglycemic Effect of Resveratrol: A Systematic Review and Meta-Analysis. Antioxidants 2021, 10, 69 .

AMA Style

Beatriz Isabel García-Martínez, Mirna Ruiz-Ramos, José Pedraza-Chaverri, Edelmiro Santiago-Osorio, Víctor Manuel Mendoza-Núñez. Hypoglycemic Effect of Resveratrol: A Systematic Review and Meta-Analysis. Antioxidants. 2021; 10 (1):69.

Chicago/Turabian Style

Beatriz Isabel García-Martínez; Mirna Ruiz-Ramos; José Pedraza-Chaverri; Edelmiro Santiago-Osorio; Víctor Manuel Mendoza-Núñez. 2021. "Hypoglycemic Effect of Resveratrol: A Systematic Review and Meta-Analysis." Antioxidants 10, no. 1: 69.

Journal article
Published: 15 November 2020 in Antioxidants
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This study aimed to assess the impact of allicin on the course of diabetic nephropathy. Study groups included control, diabetes, and diabetes-treated rats. Allicin treatment (16 mg/kg day/p.o.) started after 1 month of diabetes onset and was administered for 30 days. In the diabetes group, the systolic blood pressure (SBP) increased, also, the oxidative stress and hypoxia in the kidney cortex were evidenced by alterations in the total antioxidant capacity as well as the expression of nuclear factor (erythroid-derived 2)-like 2/Kelch ECH associating protein 1 (Nrf2/Keap1), hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), erythropoietin (Epo) and its receptor (Epo-R). Moreover, diabetes increased nephrin, and kidney injury molecule-1 (KIM-1) expression that correlated with mesangial matrix, the fibrosis index and with the expression of connective tissue growth factor (CTGF), transforming growth factor-β1 (TGF-β1), and α-smooth muscle actin (α-SMA). The insulin levels and glucose transporter protein type-4 (GLUT4) expression were decreased; otherwise, insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) expression was increased. Allicin increased Nrf2 expression and decreased SBP, Keap1, HIF-1α, and VEGF expression. Concurrently, nephrin, KIM-1, the mesangial matrix, fibrosis index, and the fibrotic proteins were decreased. Additionally, allicin decreased hyperglycemia, improved insulin levels, and prevented changes in (GLUT4) and IRSs expression induced by diabetes. In conclusion, our results demonstrate that allicin has the potential to help in the treatment of diabetic nephropathy. The cellular mechanisms underlying its effects mainly rely on the regulation of antioxidant, antifibrotic, and antidiabetic mechanisms, which can contribute towards delay in the progression of renal disease.

ACS Style

Abraham Said Arellano-Buendía; Luis Gerardo Castañeda-Lara; María L. Loredo-Mendoza; Fernando E. García-Arroyo; Pedro Rojas-Morales; Raúl Argüello-García; Juan G. Juárez-Rojas; Edilia Tapia; José Pedraza-Chaverri; Laura Gabriela Sánchez-Lozada; Horacio Osorio-Alonso. Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes. Antioxidants 2020, 9, 1134 .

AMA Style

Abraham Said Arellano-Buendía, Luis Gerardo Castañeda-Lara, María L. Loredo-Mendoza, Fernando E. García-Arroyo, Pedro Rojas-Morales, Raúl Argüello-García, Juan G. Juárez-Rojas, Edilia Tapia, José Pedraza-Chaverri, Laura Gabriela Sánchez-Lozada, Horacio Osorio-Alonso. Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes. Antioxidants. 2020; 9 (11):1134.

Chicago/Turabian Style

Abraham Said Arellano-Buendía; Luis Gerardo Castañeda-Lara; María L. Loredo-Mendoza; Fernando E. García-Arroyo; Pedro Rojas-Morales; Raúl Argüello-García; Juan G. Juárez-Rojas; Edilia Tapia; José Pedraza-Chaverri; Laura Gabriela Sánchez-Lozada; Horacio Osorio-Alonso. 2020. "Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes." Antioxidants 9, no. 11: 1134.

Journal article
Published: 27 September 2020 in Molecules
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Isoliquiritigenin (IsoLQ) is a flavonoid with antioxidant properties and inducer of endoplasmic reticulum (ER) stress. In vitro and in vivo studies show that ER stress-mediated hormesis is cytoprotective; therefore, natural antioxidants and ER stress inducers have been used to prevent renal injury. Oxidative stress and ER stress are some of the mechanisms of damage involved in cisplatin (CP)-induced nephrotoxicity. This study aims to explore whether IsoLQ pretreatment induces ER stress and produces hormesis to protect against CP-induced nephrotoxicity in Lilly Laboratories Cell-Porcine Kidney 1 (LLC-PK1) cells. During the first stage of this study, both IsoLQ protective concentration and pretreatment time against CP-induced toxicity were determined by cell viability. At the second stage, the effect of IsoLQ pretreatment on cell viability, ER stress, and oxidative stress were evaluated. IsoLQ pretreatment in CP-treated cells induces expression of glucose-related proteins 78 and 94 kDa (GRP78 and GRP94, respectively), attenuates CP-induced cell death, decreases reactive oxygen species (ROS) production, and prevents the decrease in glutathione/glutathione disulfide (GSH/GSSG) ratio, free thiols levels, and glutathione reductase (GR) activity. These data suggest that IsoLQ pretreatment has a moderately protective effect on CP-induced toxicity in LLC-PK1 cells, through ER stress-mediated hormesis, as well as by the antioxidant properties of IsoLQ.

ACS Style

Tania Gómez-Sierra; Omar Noel Medina-Campos; José D. Solano; María Elena Ibarra-Rubio; José Pedraza-Chaverri. Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells. Molecules 2020, 25, 4442 .

AMA Style

Tania Gómez-Sierra, Omar Noel Medina-Campos, José D. Solano, María Elena Ibarra-Rubio, José Pedraza-Chaverri. Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells. Molecules. 2020; 25 (19):4442.

Chicago/Turabian Style

Tania Gómez-Sierra; Omar Noel Medina-Campos; José D. Solano; María Elena Ibarra-Rubio; José Pedraza-Chaverri. 2020. "Isoliquiritigenin Pretreatment Induces Endoplasmic Reticulum Stress-Mediated Hormesis and Attenuates Cisplatin-Induced Oxidative Stress and Damage in LLC-PK1 Cells." Molecules 25, no. 19: 4442.

Journal article
Published: 24 September 2020 in Food and Chemical Toxicology
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Curcumin has protective effects in several acute kidney injury models, including that induced by potassium dichromate (K2Cr2O7). The protective effect of curcumin in this experimental model has been associated to the preservation of mitochondrial bioenergetics. This study is aimed at evaluating whether or not curcumin's protective effect in mitochondrial bioenergetics is related to the modulation of mitochondrial dynamics and biogenesis. Wistar rats were treated with a single subcutaneous dose of K2Cr2O7 (12.5 mg/kg) or received curcumin (400 mg/kg/day) by oral gavage 10 days before and one day after the K2Cr2O7 injection. K2Cr2O7 induced kidney dysfunction and increased mitochondrial hydrogen peroxide production, while decreasing the respiration directly attributable to oxidative phosphorylation and mitochondrial membrane potential. In mitochondria, K2Cr2O7 increased fission and reduced fusion. Structural analysis of mitochondria in the proximal tubular cells corroborated their fragmentation and loss of crests' integrity. Regarding mitochondrial biogenesis, K2Cr2O7 decreased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) levels. Conversely, curcumin treatment mitigated the aforementioned alterations and increased the expression of the mitochondrial transcription factor A (TFAM). Taken together, our results suggest that curcumin can protect against renal injury by modulating mitochondrial homeostasis, mitigating alterations in bioenergetics and dynamics, possibly by stimulating mitochondrial biogenesis.

ACS Style

Sabino Hazael Avila-Rojas; Omar Emiliano Aparicio-Trejo; Alfredo Briones-Herrera; Omar Noel Medina-Campos; Laura María Reyes-Fermín; Elena Martínez-Klimova; Juan Carlos León-Contreras; Rogelio Hernández-Pando; Edilia Tapia; José Pedraza-Chaverri. Alterations in mitochondrial homeostasis in a potassium dichromate model of acute kidney injury and their mitigation by curcumin. Food and Chemical Toxicology 2020, 145, 111774 .

AMA Style

Sabino Hazael Avila-Rojas, Omar Emiliano Aparicio-Trejo, Alfredo Briones-Herrera, Omar Noel Medina-Campos, Laura María Reyes-Fermín, Elena Martínez-Klimova, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Edilia Tapia, José Pedraza-Chaverri. Alterations in mitochondrial homeostasis in a potassium dichromate model of acute kidney injury and their mitigation by curcumin. Food and Chemical Toxicology. 2020; 145 ():111774.

Chicago/Turabian Style

Sabino Hazael Avila-Rojas; Omar Emiliano Aparicio-Trejo; Alfredo Briones-Herrera; Omar Noel Medina-Campos; Laura María Reyes-Fermín; Elena Martínez-Klimova; Juan Carlos León-Contreras; Rogelio Hernández-Pando; Edilia Tapia; José Pedraza-Chaverri. 2020. "Alterations in mitochondrial homeostasis in a potassium dichromate model of acute kidney injury and their mitigation by curcumin." Food and Chemical Toxicology 145, no. : 111774.

Journal article
Published: 22 September 2020 in Nutrients
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Background: Magnesium is a mineral that modulates several physiological processes. However, its relationship with intestinal microbiota has been scarcely studied. Therefore, this study aimed to assess the role of dietary magnesium content to modulate the intestinal microbiota of Wistar male rats. Methods: Rats were randomly assigned one of three diets: a control diet (C-Mg; 1000 mg/kg), a low magnesium content diet (L-Mg; 60 mg/kg), and a high magnesium content diet (H-Mg; 6000 mg/kg), for two weeks. After treatment, fecal samples were collected. Microbiota composition was assessed by sequencing the V3–V4 hypervariable region. Results: The C-Mg and L-Mg groups had more diversity than H-Mg group. CF231, SMB53, Dorea, Lactobacillus and Turibacter were enriched in the L-Mg group. In contrast, the phyla Proteobacteria, Parabacteroides, Butyricimonas, and Victivallis were overrepresented in the H-Mg group. PICRUSt analysis indicated that fecal microbiota of the L-Mg group were encoded with an increased abundance of metabolic pathways involving carbohydrate metabolism and butanoate metabolism. Conclusion: Dietary magnesium supplementation can result in intestinal dysbiosis development in a situation where there is no magnesium deficiency. Conversely, low dietary magnesium consumption is associated with microbiota with a higher capacity to harvest energy from the diet.

ACS Style

Arantxa García-Legorreta; Luis Alfonso Soriano-Pérez; Aline Mariana Flores-Buendía; Omar Noel Medina-Campos; Lilia G. Noriega; Omar Granados-Portillo; Rafael Nambo-Venegas; Armando R. Tovar; Alfredo Mendoza-Vargas; Diana Barrera-Oviedo; José Pedraza-Chaverri; Berenice Palacios-González. Effect of Dietary Magnesium Content on Intestinal Microbiota of Rats. Nutrients 2020, 12, 2889 .

AMA Style

Arantxa García-Legorreta, Luis Alfonso Soriano-Pérez, Aline Mariana Flores-Buendía, Omar Noel Medina-Campos, Lilia G. Noriega, Omar Granados-Portillo, Rafael Nambo-Venegas, Armando R. Tovar, Alfredo Mendoza-Vargas, Diana Barrera-Oviedo, José Pedraza-Chaverri, Berenice Palacios-González. Effect of Dietary Magnesium Content on Intestinal Microbiota of Rats. Nutrients. 2020; 12 (9):2889.

Chicago/Turabian Style

Arantxa García-Legorreta; Luis Alfonso Soriano-Pérez; Aline Mariana Flores-Buendía; Omar Noel Medina-Campos; Lilia G. Noriega; Omar Granados-Portillo; Rafael Nambo-Venegas; Armando R. Tovar; Alfredo Mendoza-Vargas; Diana Barrera-Oviedo; José Pedraza-Chaverri; Berenice Palacios-González. 2020. "Effect of Dietary Magnesium Content on Intestinal Microbiota of Rats." Nutrients 12, no. 9: 2889.

Journal article
Published: 20 September 2020 in Brain Sciences
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Glucose transporter (GLUT)3 up-regulation is an adaptive response activated to prevent cellular damage when brain metabolic energy is reduced. Resveratrol is a natural polyphenol with anti-oxidant and anti-inflammatory features that protects neurons against damage induced in cerebral ischemia. Since transcription factors sensitive to oxidative stress and inflammation modulate GLUT3 expression, the purpose of this work was to assess the effect of resveratrol on GLUT3 expression levels after ischemia. Male Wistar rats were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by different times of reperfusion. Resveratrol (1.9 mg/kg; i. p.) was administered at the onset of the restoration of the blood flow. Quantitative-PCR and Western blot showed that MCAO provoked a substantial increase in GLUT3 expression in the ipsilateral side to the lesion of the cerebral cortex. Immunofluorescence assays indicated that GLUT3 levels were upregulated in astrocytes. Additionally, an important increase in GLUT3 occurred in other cellular types (e.g., damaged neurons, microglia, or infiltrated macrophages). Immunodetection of the microtubule-associated protein 2 (MAP2) showed that MCAO induced severe damage to the neuronal population. However, the administration of resveratrol at the time of reperfusion resulted in injury reduction. Resveratrol also prevented the MCAO-induced increase of GLUT3 expression. In conclusion, resveratrol protects neurons from damage induced by ischemia and prevents GLUT3 upregulation in the damaged brain that might depend on AMPK activation.

ACS Style

Germán Fernando Gutiérrez Aguilar; Iván Alquisiras-Burgos; Javier Franco-Pérez; Narayana Pineda-Ramírez; Alma Ortiz-Plata; Ismael Torres; José Pedraza-Chaverri; Penélope Aguilera. Resveratrol Prevents GLUT3 Up-Regulation Induced by Middle Cerebral Artery Occlusion. Brain Sciences 2020, 10, 651 .

AMA Style

Germán Fernando Gutiérrez Aguilar, Iván Alquisiras-Burgos, Javier Franco-Pérez, Narayana Pineda-Ramírez, Alma Ortiz-Plata, Ismael Torres, José Pedraza-Chaverri, Penélope Aguilera. Resveratrol Prevents GLUT3 Up-Regulation Induced by Middle Cerebral Artery Occlusion. Brain Sciences. 2020; 10 (9):651.

Chicago/Turabian Style

Germán Fernando Gutiérrez Aguilar; Iván Alquisiras-Burgos; Javier Franco-Pérez; Narayana Pineda-Ramírez; Alma Ortiz-Plata; Ismael Torres; José Pedraza-Chaverri; Penélope Aguilera. 2020. "Resveratrol Prevents GLUT3 Up-Regulation Induced by Middle Cerebral Artery Occlusion." Brain Sciences 10, no. 9: 651.