Noemi Cardenas-Rodríguez

Dr. Noemi Cardenas-Rodríguez

Laboratorio de Neurociencias, Instituto Nacional de Pediatria, Mexico City, Ciudad de México, Mexico
orcid
Biochemistry and Molecular Biology

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 October 2008 in Food and Chemical Toxicology
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Journal Article
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José Pedraza-ChaverriJosé Pedraza-Chaverri
José Pedraza-Chaverri
Noemi Cardenas-RodríguezNoemi Cardenas-Rodríguez
Noemi Cardenas-Rodríguez
Marisol Orozco-IbarraMarisol Orozco-Ibarra
Marisol Orozco-Ibarra
Jazmin Marlen Pérez RojasJazmin Marlen Pérez Rojas
Jazmin Marlen Pérez Rojas

7 October 2022 in Cells
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Journal Article
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BFBerenice Franco-Juárez
Berenice Franco-Juárez
CCCristina Coronel-Cruz
Cristina Coronel-Cruz
BHBeatriz Hernández
Beatriz Hernández
SGSaul Gomez-Manzo
Saul Gomez-Manzo
Noemi Cardenas-RodríguezNoemi Cardenas-Rodríguez
Noemi Cardenas-Rodríguez
DODaniel Ortega-Cuellar
Daniel Ortega-Cuellar
Transcription factor EB (TFEB) is considered the master transcriptional regulator of autophagy and lysosomal biogenesis, which regulates target gene expression through binding to CLEAR motifs. TFEB dysregulation has been linked to the development of numerous pathological conditions; however, several other lines of evidence show that TFEB might be a point of convergence of diverse signaling pathways and might therefore modulate other important biological processes such as cellular senescence, DNA repair, ER stress, carbohydrates, and lipid metabolism and WNT signaling-related processes. The regulation of TFEB occurs predominantly at the post-translational level, including phosphorylation, acetylation, SUMOylating, PARsylation, and glycosylation. It is noteworthy that TFEB activation is context-dependent; therefore, its regulation is subjected to coordinated mechanisms that respond not only to nutrient fluctuations but also to stress cell programs to ensure proper cell homeostasis and organismal health. In this review, we provide updated insights into novel post-translational modifications that regulate TFEB activity and give an overview of TFEB beyond its widely known role in autophagy and the lysosomal pathway, thus opening the possibility of considering TFEB as a potential therapeutic target.

13 April 2022 in Pharmaceuticals
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ICItzel Jatziri Contreras
Itzel Jatziri Contreras
Noemi Cardenas-RodríguezNoemi Cardenas-Rodríguez
Noemi Cardenas-Rodríguez
Antonio Romo-MancillasAntonio Romo-Mancillas
Antonio Romo-Mancillas
Cindy BandalaCindy Bandala
Cindy Bandala
SZSergio R Zamudio
Sergio R Zamudio
LMLuz Adriana Pichardo- Macías
Luz Adriana Pichardo- Macías
Epilepsy is a chronic disease that affects millions of people worldwide. Antiepileptic drugs (AEDs) are used to control seizures. Even though parts of their mechanisms of action are known, there are still components that need to be studied. Therefore, the search for novel drugs, new molecular targets, and a better understanding of the mechanisms of action of existing drugs is still crucial. Levetiracetam (LEV) is an AED that has been shown to be effective in seizure control and is well-tolerable, with a novel mechanism of action through an interaction with the synaptic vesicle protein 2A (SV2A). Moreover, LEV has other molecular targets that involve calcium homeostasis, the GABAergic system, and AMPA receptors among others, that might be integrated into a single mechanism of action that could explain the antiepileptogenic, anti-inflammatory, neuroprotective, and antioxidant properties of LEV. This puts it as a possible multitarget drug with clinical applications other than for epilepsy. According to the above, the objective of this work was to carry out a comprehensive and integrative review of LEV in relation to its clinical uses, structural properties, therapeutical targets, and different molecular, genetic, and systemic action mechanisms in order to consider LEV as a candidate for drug repurposing.

Verified
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Noemi Cardenas-RodríguezNoemi Cardenas-Rodríguez
Noemi Cardenas-Rodríguez
BHBernardino Huerta-Gertrudis
Bernardino Huerta-Gertrudis
LRLiliana Rivera-Espinosa
Liliana Rivera-Espinosa
HCHortencia Montesinos Correa
Hortencia Montesinos Correa
Cindy BandalaCindy Bandala
Cindy Bandala
ECElvia Coballase
Elvia Coballase
Oxidative stress, a state of imbalance in the production of reactive oxygen species and nitrogen, is induced by a wide variety of factors. This biochemical state is associated with systemic diseases, and diseases affecting the central nervous system. Epilepsy is a chronic neurological disorder with refractoriness to drug therapy at about 30%. Currently, experimental evidence supports the involvement of oxidative stress in seizures, in the process of their generation, and in the mechanisms associated with refractoriness to drug therapy. Hence, the aim of this review is to present information in order to facilitate the handling of this evidence and determine the therapeutic impact of the biochemical status for this pathology.

1 January 2006 in Free Radical Research
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Journal Article
Closed access
EFEsaú Floriano-Sánchez
Esaú Floriano-Sánchez
CVCleva Villanueva
Cleva Villanueva
OMOmar Noel Medina-Campos
Omar Noel Medina-Campos
DRDiana Rocha-Mendoza
Diana Rocha-Mendoza
Dolores Javier Sánchez GonzálezDolores Javier Sánchez González
Dolores Javier Sánchez González
José Pedraza-ChaverriJosé Pedraza-Chaverri
José Pedraza-Chaverri
The antioxidant nordihydroguaiaretic acid (NDGA) has recently become well known as a putative anticancer drug. In this paper, it was evaluated the in vitro peroxynitrite (ONOO− ), singlet oxygen (1O2), hydroxyl radical (OH√), hydrogen peroxide (H2O2), superoxide anion and hypochlorous acid (HOCl) scavenging capacity of NDGA. It was found that NDGA scavenges: (a) ONOO− (IC50 = 4 ± 0.94 μM) as efficiently as uric acid; (b) 1O2 (IC50 = 151 ± 20 μM) more efficiently than dimethyl thiourea, lipoic acid, N-acetyl-cysteine and glutathione; (c) OH√ (IC50 = 0.15 ± 0.02 μM) more efficiently than dimethyl thiourea, uric acid, trolox, dimethyl sulfoxide and mannitol, (d) (IC50 = 15 ± 1 μM) more efficiently than N-acetyl-cysteine, glutathione, tempol and deferoxamine and (e) HOCl (IC50 = 622 ± 42 μM) as efficiently as lipoic acid and N-acetyl-cysteine. NDGA was unable to scavenge H2O2. In an in vivo study in rats, NDGA was able to prevent ozone-induced tyrosine nitration in lungs. It is concluded that NDGA is a potent in vitro scavenger of ONOO− , 1O2, OH√, and HOCl and is able to prevent lung tyrosine nitration in vivo.

18 May 2014 in Oxidative Medicine and Cellular Longevity
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EMElizabeth Moreno-Arriola
Elizabeth Moreno-Arriola
Noemi Cardenas-RodríguezNoemi Cardenas-Rodríguez
Noemi Cardenas-Rodríguez
ECElvia Coballase-Urrutia
Elvia Coballase-Urrutia
JPJosé Pedraza-Chaverri
José Pedraza-Chaverri
LCLiliana Carmona-Aparicio
Liliana Carmona-Aparicio
DODaniel Ortega
Daniel Ortega
Caenorhabditis elegansis a powerful model organism that is invaluable for experimental research because it can be used to recapitulate most human diseases at either the metabolic or genomic levelin vivo. This organism contains many key components related to metabolic and oxidative stress networks that could conceivably allow us to increase and integrate information to understand the causes and mechanisms of complex diseases. Oxidative stress is an etiological factor that influences numerous human diseases, including diabetes.C. elegansdisplays remarkably similar molecular bases and cellular pathways to those of mammals. Defects in the insulin/insulin-like growth factor-1 signaling pathway or increased ROS levels induce the conserved phase II detoxification response via the SKN-1 pathway to fight against oxidative stress. However, it is noteworthy that, aside from the detrimental effects of ROS, they have been proposed as second messengers that trigger the mitohormetic response to attenuate the adverse effects of oxidative stress. Herein, we briefly describe the importance ofC. elegansas an experimental model system for studying metabolic disorders related to oxidative stress and the molecular mechanisms that underlie their pathophysiology.