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Dr. Nicoletta Filigheddu
Department of Translational Medicine, University of Piemonte Orientale, Novara, Italy

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0 Signal Transduction
0 Muscle regeneration
0 muscle atrophy
0 ghrelin
0 Satellite cells

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ghrelin
muscle atrophy
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Satellite cells

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Review
Published: 02 June 2021 in Cells
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Growth hormone (GH) and insulin-like growth factor-1 (IGF-I) are pleiotropic hormones with important roles in lifespan. They promote growth, anabolic actions, and body maintenance, and in conditions of energy deprivation, favor catabolic feedback mechanisms switching from carbohydrate oxidation to lipolysis, with the aim to preserve protein storages and survival. IGF-I/insulin signaling was also the first one identified in the regulation of lifespan in relation to the nutrient-sensing. Indeed, nutrients are crucial modifiers of the GH/IGF-I axis, and these hormones also regulate the complex orchestration of utilization of nutrients in cell and tissues. The aim of this review is to summarize current knowledge on the reciprocal feedback among the GH/IGF-I axis, macro and micronutrients, and dietary regimens, including caloric restriction. Expanding the depth of information on this topic could open perspectives in nutrition management, prevention, and treatment of GH/IGF-I deficiency or excess during life.

ACS Style

Marina Caputo; Stella Pigni; Emanuela Agosti; Tommaso Daffara; Alice Ferrero; Nicoletta Filigheddu; Flavia Prodam. Regulation of GH and GH Signaling by Nutrients. Cells 2021, 10, 1376 .

AMA Style

Marina Caputo, Stella Pigni, Emanuela Agosti, Tommaso Daffara, Alice Ferrero, Nicoletta Filigheddu, Flavia Prodam. Regulation of GH and GH Signaling by Nutrients. Cells. 2021; 10 (6):1376.

Chicago/Turabian Style

Marina Caputo; Stella Pigni; Emanuela Agosti; Tommaso Daffara; Alice Ferrero; Nicoletta Filigheddu; Flavia Prodam. 2021. "Regulation of GH and GH Signaling by Nutrients." Cells 10, no. 6: 1376.

Journal article
Published: 22 February 2021 in Aging
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We previously determined that different vitamin D metabolites can have opposite effects on C2C12 myotubes, depending on the sites of hydroxylation or doses. Specifically, 25(OH)D3 (25VD) has an anti-atrophic activity, 1,25(OH)2D3 induces atrophy, and 24,25(OH)2D3 is anti-atrophic at low concentrations and atrophic at high concentrations. This study aimed to clarify whether cholecalciferol (VD3) too, the non-hydroxylated upstream metabolite, has a direct effect on muscle cells.

ACS Style

Maraiza Alves Teixeira; Marilisa De Feudis; Simone Reano; Tommaso Raiteri; Andrea Scircoli; Ivan Zaggia; Sara Ruga; Laura Salvadori; Flavia Prodam; Paolo Marzullo; Claudio Molinari; Davide Corà; Nicoletta Filigheddu. Cholecalciferol (vitamin D3) has a direct protective activity against interleukin 6-induced atrophy in C2C12 myotubes. Aging 2021, 13, 4895 -4910.

AMA Style

Maraiza Alves Teixeira, Marilisa De Feudis, Simone Reano, Tommaso Raiteri, Andrea Scircoli, Ivan Zaggia, Sara Ruga, Laura Salvadori, Flavia Prodam, Paolo Marzullo, Claudio Molinari, Davide Corà, Nicoletta Filigheddu. Cholecalciferol (vitamin D3) has a direct protective activity against interleukin 6-induced atrophy in C2C12 myotubes. Aging. 2021; 13 (4):4895-4910.

Chicago/Turabian Style

Maraiza Alves Teixeira; Marilisa De Feudis; Simone Reano; Tommaso Raiteri; Andrea Scircoli; Ivan Zaggia; Sara Ruga; Laura Salvadori; Flavia Prodam; Paolo Marzullo; Claudio Molinari; Davide Corà; Nicoletta Filigheddu. 2021. "Cholecalciferol (vitamin D3) has a direct protective activity against interleukin 6-induced atrophy in C2C12 myotubes." Aging 13, no. 4: 4895-4910.

Review
Published: 30 July 2020 in Nutrients
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Background: Global dietary patterns have gradually shifted toward a ‘western type’ with progressive increases in rates of metabolic imbalance. Recently, animal and human studies have revealed positive effects of caloric restriction (CR) on many health domains, giving new knowledge for prevention of ill and health promotion; Methods: We conducted a systematic review (SR) of randomized controlled trials (RCTs) investigating the role of CR on health status in adults. A meta-analysis was performed on anthropometric, cardiovascular and metabolic outcomes; Results: A total of 29 articles were retrieved including data from eight RCTs. All included RCTs were at low risk for performance bias related to objective outcomes. Collectively, articles included 704 subjects. Among the 334 subjects subjected to CR, the compliance with the intervention appeared generally high. Meta-analyses proved benefit of CR on reduction of body weight, BMI, fat mass, total cholesterol, while a minor impact was shown for LDL, fasting glucose and insulin levels. No effect emerged for HDL and blood pressure after CR. Data were insufficient for other hormone variables in relation to meta-analysis of CR effects; Conclusion: CR is a nutritional pattern linked to improved cardiometabolic status. However, evidence is limited on the multidimensional aspects of health and requires more studies of high quality to identify the precise impact of CR on health status and longevity.

ACS Style

Silvia Caristia; Marta Vito; Andrea Sarro; Alessio Leone; Alessandro Pecere; Angelica Zibetti; Nicoletta Filigheddu; Patrizia Zeppegno; Flavia Prodam; Fabrizio Faggiano; Paolo Marzullo. Is Caloric Restriction Associated with Better Healthy Aging Outcomes? A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutrients 2020, 12, 2290 .

AMA Style

Silvia Caristia, Marta Vito, Andrea Sarro, Alessio Leone, Alessandro Pecere, Angelica Zibetti, Nicoletta Filigheddu, Patrizia Zeppegno, Flavia Prodam, Fabrizio Faggiano, Paolo Marzullo. Is Caloric Restriction Associated with Better Healthy Aging Outcomes? A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Nutrients. 2020; 12 (8):2290.

Chicago/Turabian Style

Silvia Caristia; Marta Vito; Andrea Sarro; Alessio Leone; Alessandro Pecere; Angelica Zibetti; Nicoletta Filigheddu; Patrizia Zeppegno; Flavia Prodam; Fabrizio Faggiano; Paolo Marzullo. 2020. "Is Caloric Restriction Associated with Better Healthy Aging Outcomes? A Systematic Review and Meta-Analysis of Randomized Controlled Trials." Nutrients 12, no. 8: 2290.

Journal article
Published: 26 July 2020 in Aging
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Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with anti-atrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene (Ghrl KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation. Yet, the aging of Tg and Ghrl KO mice occurs with different dynamics: while old Tg mice seem to preserve the characteristics of young animals, Ghrl KO mice features deteriorate with aging. However, young Ghrl KO mice show more favorable traits compared to WT animals that result, on the whole, in better performances in aged Ghrl KO animals. Treatment with pharmacological doses of UnAG improved muscle performance in old mice without modifying the feeding behavior, body weight, and adipose tissue mass. The antiatrophic effect on muscle mass did not correlate with modifications of protein catabolism. However, UnAG treatment induced a strong shift towards oxidative metabolism in muscle. Altogether, these data confirmed and expanded some of the previously reported findings and advocate for the design of UnAG analogs to treat sarcopenia.

ACS Style

Emanuela Agosti; Marilisa De Feudis; Elia Angelino; Roberta Belli; Maraiza Alves Teixeira; Ivan Zaggia; Edoardo Tamiso; Tommaso Raiteri; Andrea Scircoli; Flavio L. Ronzoni; Maurizio Muscaritoli; Andrea Graziani; Flavia Prodam; Maurilio Sampaolesi; Paola Costelli; Elisabetta Ferraro; Simone Reano; Nicoletta Filigheddu. Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice. Aging 2020, 12, 13939 -13957.

AMA Style

Emanuela Agosti, Marilisa De Feudis, Elia Angelino, Roberta Belli, Maraiza Alves Teixeira, Ivan Zaggia, Edoardo Tamiso, Tommaso Raiteri, Andrea Scircoli, Flavio L. Ronzoni, Maurizio Muscaritoli, Andrea Graziani, Flavia Prodam, Maurilio Sampaolesi, Paola Costelli, Elisabetta Ferraro, Simone Reano, Nicoletta Filigheddu. Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice. Aging. 2020; 12 (14):13939-13957.

Chicago/Turabian Style

Emanuela Agosti; Marilisa De Feudis; Elia Angelino; Roberta Belli; Maraiza Alves Teixeira; Ivan Zaggia; Edoardo Tamiso; Tommaso Raiteri; Andrea Scircoli; Flavio L. Ronzoni; Maurizio Muscaritoli; Andrea Graziani; Flavia Prodam; Maurilio Sampaolesi; Paola Costelli; Elisabetta Ferraro; Simone Reano; Nicoletta Filigheddu. 2020. "Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice." Aging 12, no. 14: 13939-13957.

Review
Published: 06 October 2019 in Nutrients
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Background: The association between circulating levels of vitamin D and the incidence of chronic diseases is known. The identification of vitamin D as a biomarker of physiological/pathological ageing could contribute to expanding current knowledge of its involvement in healthy ageing. Methods: According to PRISMA guidelines, a systematic review was conducted on cohorts studying the role of 25OH-Vitamin D [25(OH)D] and 1,25(OH)2-Vitamin D [1,25(OH)2D] concentrations as biomarkers of healthy ageing. We consulted MedLine, Scopus, and Web of Science to search for studies on the association between vitamin D status in populations of originally healthy adults, and outcomes of longevity, illness, and physical and cognitive functionality. The quality of the studies was assessed using the Newcastle Ottawa scale. Results: Twenty cohorts from 24 articles were selected for this review. Inverse associations were found between low 25(OH)D levels and all-cause mortality, respiratory and cardiovascular events, as well as markers relating to hip and non-vertebral fractures. Associations between 1,25(OH)2D and healthy ageing outcomes gave similar results, although of lower clinical significance. Conclusions: This systematic review pinpoints peculiar aspects of vitamin D as a multidimensional predictor of ill health in the ageing process. Further well-designed controlled trials to investigate whether vitamin D supplement results in superior outcomes are warranted in the future.

ACS Style

Silvia Caristia; Nicoletta Filigheddu; Francesco Barone-Adesi; Andrea Sarro; Tommaso Testa; Corrado Magnani; Gianluca Aimaretti; Fabrizio Faggiano; Paolo Marzullo; Barone- Adesi. Vitamin D as a Biomarker of Ill Health among the Over-50s: A Systematic Review of Cohort Studies. Nutrients 2019, 11, 2384 .

AMA Style

Silvia Caristia, Nicoletta Filigheddu, Francesco Barone-Adesi, Andrea Sarro, Tommaso Testa, Corrado Magnani, Gianluca Aimaretti, Fabrizio Faggiano, Paolo Marzullo, Barone- Adesi. Vitamin D as a Biomarker of Ill Health among the Over-50s: A Systematic Review of Cohort Studies. Nutrients. 2019; 11 (10):2384.

Chicago/Turabian Style

Silvia Caristia; Nicoletta Filigheddu; Francesco Barone-Adesi; Andrea Sarro; Tommaso Testa; Corrado Magnani; Gianluca Aimaretti; Fabrizio Faggiano; Paolo Marzullo; Barone- Adesi. 2019. "Vitamin D as a Biomarker of Ill Health among the Over-50s: A Systematic Review of Cohort Studies." Nutrients 11, no. 10: 2384.

Scholarlyarticle
Published: 19 June 2019 in The Journal of Clinical Endocrinology & Metabolism
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Background GH deficiency (GHD) is characterized by a cluster of cardiovascular risk factors and subtle inflammation. We aimed to demonstrate, through a proteomic approach, molecules directly modulated by GHD and involved in the inflammatory state. Methods Ten children with isolated GHD were studied before and after 1 year of treatment with rhGH and compared with 14 matched controls. A two-dimensional electrophoresis plasma proteomics analysis was performed at baseline and after GH treatment to identify the top molecules modulated by GH. In vitro studies on human hepatoma (HepG2) cells were performed to validate the data. Results Twelve of 20 proteomic spots were predicted to be isoforms α and β of haptoglobin (Hp) and confirmed by liquid chromatography tandem mass spectrometry and Western immunoblot analyses. Hp levels were higher in patients with GHD than controls at baseline (P < 0.001) and were reduced following GH treatment (P < 0.01). In HepG2 cells, both GH and IGF-1 were able to downregulate IL-6–induced Hp secretion. Moreover, Hp secretion was restored in pegvisomant-treated HepG2 cells. Conclusions Hp is a molecule acting in the inflammatory state of GHD and a possible biomarker for GH treatment. Nevertheless, the contribution of other factors and the molecular pathways involved in the GH downregulation of Hp remain to be clearly defined.

ACS Style

Marilisa De Feudis; Gillian Elisabeth Walker; Giulia Genoni; Marcello Manfredi; Emanuela Agosti; Mara Giordano; Marina Caputo; Luisa Di Trapani; Emilio Marengo; Gianluca Aimaretti; Nicoletta Filigheddu; Simonetta Bellone; Gianni Bona; Flavia Prodam. Identification of Haptoglobin as a Readout of rhGH Therapy in GH Deficiency. The Journal of Clinical Endocrinology & Metabolism 2019, 104, 5263 -5273.

AMA Style

Marilisa De Feudis, Gillian Elisabeth Walker, Giulia Genoni, Marcello Manfredi, Emanuela Agosti, Mara Giordano, Marina Caputo, Luisa Di Trapani, Emilio Marengo, Gianluca Aimaretti, Nicoletta Filigheddu, Simonetta Bellone, Gianni Bona, Flavia Prodam. Identification of Haptoglobin as a Readout of rhGH Therapy in GH Deficiency. The Journal of Clinical Endocrinology & Metabolism. 2019; 104 (11):5263-5273.

Chicago/Turabian Style

Marilisa De Feudis; Gillian Elisabeth Walker; Giulia Genoni; Marcello Manfredi; Emanuela Agosti; Mara Giordano; Marina Caputo; Luisa Di Trapani; Emilio Marengo; Gianluca Aimaretti; Nicoletta Filigheddu; Simonetta Bellone; Gianni Bona; Flavia Prodam. 2019. "Identification of Haptoglobin as a Readout of rhGH Therapy in GH Deficiency." The Journal of Clinical Endocrinology & Metabolism 104, no. 11: 5263-5273.

Regular paper
Published: 04 March 2019 in Acta Physiologica
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Aim Loss of skeletal muscle is one of the main features of cancer cachexia. Vitamin D (VD) deficiency is associated with impairment of muscle mass and performance and is highly prevalent in cachectic patients; therefore, VD supplementation has been proposed to counteract cancer cachexia‐associated muscle loss. However, in both cachectic cancer patients and tumour‐bearing animals, VD supplementation led to disappointing results, urging the need for a better understanding of VD activity on skeletal muscle. Methods Cancer‐associated muscle wasting was reproduced in vitro by treating C2C12 myotubes with cancer cell conditioned medium, a combination of TNF‐α and IFNγ or IL‐6 pro‐cachectic cytokines. The biological effects and mechanisms of action of 1,25‐dihydroxy VD (1,25 VD) and its precursor 25‐hydroxy VD (25 VD) on myotubes were explored. Results We demonstrated that only 25 VD was able to protect from atrophy by activating Akt signalling, inducing protein synthesis, and stimulating the autophagic flux, while 1,25 VD had an atrophic activity per se, increasing FoxO3 levels, inducing the expression of atrogenes, and blocking the autophagic flux. Furthermore, we showed that the contrasting activities of these VD metabolites on C2C12 myotubes depend on a differential induction of VD‐24‐hydroxylase and transformation of VD metabolites in pro‐atrophic 24‐hydroxylated products, as silencing of VD‐24‐hydroxylase reduced the atrophic activity of 1,25 VD. Conclusions Altogether these data might explain the lack of efficacy of VD treatment in vivo for the protection of muscle mass in cancer. This article is protected by copyright. All rights reserved.

ACS Style

Hana Sustova; Marilisa De Feudis; Simone Reano; Maraiza Alves Teixeira; Ilaria Valle; Ivan Zaggia; Emanuela Agosti; Flavia Prodam; Nicoletta Filigheddu. Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D3 on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes. Acta Physiologica 2019, 226, e13269 .

AMA Style

Hana Sustova, Marilisa De Feudis, Simone Reano, Maraiza Alves Teixeira, Ilaria Valle, Ivan Zaggia, Emanuela Agosti, Flavia Prodam, Nicoletta Filigheddu. Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D3 on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes. Acta Physiologica. 2019; 226 (3):e13269.

Chicago/Turabian Style

Hana Sustova; Marilisa De Feudis; Simone Reano; Maraiza Alves Teixeira; Ilaria Valle; Ivan Zaggia; Emanuela Agosti; Flavia Prodam; Nicoletta Filigheddu. 2019. "Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D3 on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes." Acta Physiologica 226, no. 3: e13269.

Journal article
Published: 01 January 2019 in Disease Models & Mechanisms
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STIM and ORAI proteins play a fundamental role in calcium signalling, allowing for calcium influx through the plasma membrane upon depletion of intracellular stores in a process known as Store Operated Ca2+ Entry. Point mutations that lead to gain-of-function activity of either STIM1 or ORAI1 are responsible for a cluster of ultra-rare syndromes characterized by motor disturbances and platelet dysfunction. The prevalence of these disorders is at present unknown. In the present contribution, we describe the generation and characterization of a knock-in mouse model (KI-STIM1I115F) that bears a clinically relevant mutation located in one of the two calcium-sensing EF-hand motifs of STIM1. The mouse colony is viable and fertile. Myotubes from these mice show an increased Store Operated Ca2+ Entry, as predicted. This most likely causes the dystrophic muscle phenotype observed, which worsens with age. Such histological features are not accompanied by a significant creatine kinase increase. Yet, animals have a significantly worst performance in the rotarod and treadmill tests, showing an increased susceptibility to fatigue, in analogy to the human disease. The mice also show an increased bleeding time and thrombocytopenia, as well as an unexpected defect in the myeloid lineage and in natural killer cells. The present model, together with the recently described models bearing the R304W mutation (located on the coiled-coil domain in the cytosolic side of STIM1), represents an ideal platform to characterize the disorder and test therapeutic strategies for patients with STIM1 mutations, currently without therapeutic solutions.

ACS Style

Celia Cordero-Sanchez; Beatrice Riva; Simone Reano; Nausicaa Clemente; Ivan Zaggia; Federico A. Ruffinatti; Alberto Potenzieri; Tracey Pirali; Salvatore Raffa; Sabina Sangaletti; Mario P. Colombo; Alessandra Bertoni; Matteo Garibaldi; Nicoletta Filigheddu; Armando A. Genazzani. A luminal EF-hand mutation in STIM1 in mice causes the clinical hallmarks of tubular aggregate myopathy. Disease Models & Mechanisms 2019, 13, 1 .

AMA Style

Celia Cordero-Sanchez, Beatrice Riva, Simone Reano, Nausicaa Clemente, Ivan Zaggia, Federico A. Ruffinatti, Alberto Potenzieri, Tracey Pirali, Salvatore Raffa, Sabina Sangaletti, Mario P. Colombo, Alessandra Bertoni, Matteo Garibaldi, Nicoletta Filigheddu, Armando A. Genazzani. A luminal EF-hand mutation in STIM1 in mice causes the clinical hallmarks of tubular aggregate myopathy. Disease Models & Mechanisms. 2019; 13 (2):1.

Chicago/Turabian Style

Celia Cordero-Sanchez; Beatrice Riva; Simone Reano; Nausicaa Clemente; Ivan Zaggia; Federico A. Ruffinatti; Alberto Potenzieri; Tracey Pirali; Salvatore Raffa; Sabina Sangaletti; Mario P. Colombo; Alessandra Bertoni; Matteo Garibaldi; Nicoletta Filigheddu; Armando A. Genazzani. 2019. "A luminal EF-hand mutation in STIM1 in mice causes the clinical hallmarks of tubular aggregate myopathy." Disease Models & Mechanisms 13, no. 2: 1.

Original article
Published: 30 May 2018 in Endocrine
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Muscle regeneration depends on satellite cells (SCs), quiescent precursors that, in consequence of injury or pathological states such as muscular dystrophies, activate, proliferate, and differentiate to repair the damaged tissue. A subset of SCs undergoes self-renewal, thus preserving the SC pool and its regenerative potential. The peptides produced by the ghrelin gene, i.e., acylated ghrelin (AG), unacylated ghrelin (UnAG), and obestatin (Ob), affect skeletal muscle biology in several ways, not always with overlapping effects. In particular, UnAG and Ob promote SC self-renewal and myoblast differentiation, thus fostering muscle regeneration. To delineate the endogenous contribution of preproghrelin in muscle regeneration, we evaluated the repair process in Ghrl−/− mice upon CTX-induced injury. Although muscles from Ghrl−/− mice do not visibly differ from WT muscles in term of weight, structure, and SCs content, muscle regeneration after CTX-induced injury is impaired in Ghrl−/− mice, indicating that ghrelin-derived peptides actively participate in muscle repair. Remarkably, the lack of ghrelin gene impacts SC self-renewal during regeneration. Although we cannot discern the specific Ghrl-derived peptide responsible for such activities, these data indicate that Ghrl contributes to a proper muscle regeneration.

ACS Style

Elia Angelino; Simone Reano; Alessandro Bollo; Michele Ferrara; Marilisa De Feudis; Hana Sustova; Emanuela Agosti; Sara Clerici; Flavia Prodam; Catherine-Laure Tomasetto; Andrea Graziani; Nicoletta Filigheddu. Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal. Endocrine 2018, 62, 129 -135.

AMA Style

Elia Angelino, Simone Reano, Alessandro Bollo, Michele Ferrara, Marilisa De Feudis, Hana Sustova, Emanuela Agosti, Sara Clerici, Flavia Prodam, Catherine-Laure Tomasetto, Andrea Graziani, Nicoletta Filigheddu. Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal. Endocrine. 2018; 62 (1):129-135.

Chicago/Turabian Style

Elia Angelino; Simone Reano; Alessandro Bollo; Michele Ferrara; Marilisa De Feudis; Hana Sustova; Emanuela Agosti; Sara Clerici; Flavia Prodam; Catherine-Laure Tomasetto; Andrea Graziani; Nicoletta Filigheddu. 2018. "Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal." Endocrine 62, no. 1: 129-135.

Research article
Published: 26 February 2018 in Oxidative Medicine and Cellular Longevity
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Cancer cachexia is a devastating syndrome occurring in the majority of terminally ill cancer patients. Notably, skeletal muscle atrophy is a consistent feature affecting the quality of life and prognosis. To date, limited therapeutic options are available, and research in the field is hampered by the lack of satisfactory models to study the complexity of wasting in cachexia-inducing tumors, such as pancreatic cancer. Moreover, currently used in vivo models are characterized by an explosive cachexia with a lethal wasting within few days, while pancreatic cancer patients might experience alterations long before the onset of overt wasting. In this work, we established and characterized a slow-paced model of pancreatic cancer-induced muscle wasting that promotes efficient muscular wasting in vitro and in vivo. Treatment with conditioned media from pancreatic cancer cells led to the induction of atrophy in vitro, while tumor-bearing mice presented a clear reduction in muscle mass and functionality. Intriguingly, several metabolic alterations in tumor-bearing mice were identified, paving the way for therapeutic interventions with drugs targeting metabolism.

ACS Style

Elisabeth Wyart; Simone Reano; Myriam Y. Hsu; Dario Livio Longo; Mingchuan Li; Emilio Hirsch; Nicoletta Filigheddu; Alessandra Ghigo; Chiara Riganti; Paolo Ettore Porporato. Metabolic Alterations in a Slow-Paced Model of Pancreatic Cancer-Induced Wasting. Oxidative Medicine and Cellular Longevity 2018, 2018, 1 -10.

AMA Style

Elisabeth Wyart, Simone Reano, Myriam Y. Hsu, Dario Livio Longo, Mingchuan Li, Emilio Hirsch, Nicoletta Filigheddu, Alessandra Ghigo, Chiara Riganti, Paolo Ettore Porporato. Metabolic Alterations in a Slow-Paced Model of Pancreatic Cancer-Induced Wasting. Oxidative Medicine and Cellular Longevity. 2018; 2018 ():1-10.

Chicago/Turabian Style

Elisabeth Wyart; Simone Reano; Myriam Y. Hsu; Dario Livio Longo; Mingchuan Li; Emilio Hirsch; Nicoletta Filigheddu; Alessandra Ghigo; Chiara Riganti; Paolo Ettore Porporato. 2018. "Metabolic Alterations in a Slow-Paced Model of Pancreatic Cancer-Induced Wasting." Oxidative Medicine and Cellular Longevity 2018, no. : 1-10.

Journal article
Published: 01 January 2018 in BIO-PROTOCOL
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Satellite cell (SC) transplantation represents a powerful strategy to investigate SC biology during muscle regeneration. We described here a protocol for SC isolation from green fluorescent protein (GFP)-expressing mice and their transplantation into murine muscles. This procedure was originally used to assess the effects of the hormone unacylated ghrelin on muscle regeneration, in particular evaluating how the increase of unacylated ghrelin in the recipient muscle affected the engraftment of donor SCs (Reano et al., 2017). Bio-protocol is an online peer-reviewed protocol journal. Its mission is to make life science research more efficient and reproducible by curating and hosting high quality, free access protocols.

ACS Style

Elia Angelino; Simone Reano; Michele Ferrara; Emanuela Agosti; Hana Sustova; Valeria Malacarne; Sara Clerici; Andrea Graziani; Nicoletta Filigheddu. Mouse Satellite Cell Isolation and Transplantation. BIO-PROTOCOL 2018, 8, 1 .

AMA Style

Elia Angelino, Simone Reano, Michele Ferrara, Emanuela Agosti, Hana Sustova, Valeria Malacarne, Sara Clerici, Andrea Graziani, Nicoletta Filigheddu. Mouse Satellite Cell Isolation and Transplantation. BIO-PROTOCOL. 2018; 8 (2):1.

Chicago/Turabian Style

Elia Angelino; Simone Reano; Michele Ferrara; Emanuela Agosti; Hana Sustova; Valeria Malacarne; Sara Clerici; Andrea Graziani; Nicoletta Filigheddu. 2018. "Mouse Satellite Cell Isolation and Transplantation." BIO-PROTOCOL 8, no. 2: 1.

Review
Published: 08 December 2017 in Cell Research
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Glycolysis has long been considered as the major metabolic process for energy production and anabolic growth in cancer cells. Although such a view has been instrumental for the development of powerful imaging tools that are still used in the clinics, it is now clear that mitochondria play a key role in oncogenesis. Besides exerting central bioenergetic functions, mitochondria provide indeed building blocks for tumor anabolism, control redox and calcium homeostasis, participate in transcriptional regulation, and govern cell death. Thus, mitochondria constitute promising targets for the development of novel anticancer agents. However, tumors arise, progress, and respond to therapy in the context of an intimate crosstalk with the host immune system, and many immunological functions rely on intact mitochondrial metabolism. Here, we review the cancer cell-intrinsic and cell-extrinsic mechanisms through which mitochondria influence all steps of oncogenesis, with a focus on the therapeutic potential of targeting mitochondrial metabolism for cancer therapy.

ACS Style

Paolo Ettore Porporato; Nicoletta Filigheddu; Jose Manuel Bravo-San Pedro; Guido Kroemer; Lorenzo Galluzzi. Mitochondrial metabolism and cancer. Cell Research 2017, 28, 265 -280.

AMA Style

Paolo Ettore Porporato, Nicoletta Filigheddu, Jose Manuel Bravo-San Pedro, Guido Kroemer, Lorenzo Galluzzi. Mitochondrial metabolism and cancer. Cell Research. 2017; 28 (3):265-280.

Chicago/Turabian Style

Paolo Ettore Porporato; Nicoletta Filigheddu; Jose Manuel Bravo-San Pedro; Guido Kroemer; Lorenzo Galluzzi. 2017. "Mitochondrial metabolism and cancer." Cell Research 28, no. 3: 265-280.

Review
Published: 01 December 2017 in Current Opinion in Supportive & Palliative Care
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The possibility to use vitamin D supplementation to improve muscle wasting, with particular focus on cancer cachexia, is discussed. Vitamin D exerts biological actions on myogenic precursor proliferation and differentiation, impinging on muscle regeneration. However, the effects of VitD supplementation in diseases associated with muscle atrophy, such as cancer cachexia, are poorly investigated. Data obtained in experimental models of cancer cachexia show that the administration of vitamin D to tumor-bearing animals is not able to prevent or delay both muscle wasting and adipose tissue depletion, despite increased expression of muscle vitamin D receptor. Not just vitamin D supplementation impairs muscle damage-induced regeneration, suggesting that upregulation of vitamin D receptor signaling could contribute to muscle wasting. Vitamin D supplementation is likely beneficial to reduce or delay aging-related sarcopenia and osteoporosis, although the available data still put in evidence significant discrepancies. By contrast, VitD supplementation to tumor-bearing animals or to rats with arthritis was shown to be totally ineffective. In this regard, the adoption of VitD treatment in patients with cancer cachexia or other chronic diseases should be carefully evaluated, in particular whenever a regenerative process might be involved.

ACS Style

Fabio Penna; Andrea Camperi; Maurizio Muscaritoli; Nicoletta Filigheddu; Paola Costelli. The role of vitamin D in cancer cachexia. Current Opinion in Supportive & Palliative Care 2017, 11, 287 -292.

AMA Style

Fabio Penna, Andrea Camperi, Maurizio Muscaritoli, Nicoletta Filigheddu, Paola Costelli. The role of vitamin D in cancer cachexia. Current Opinion in Supportive & Palliative Care. 2017; 11 (4):287-292.

Chicago/Turabian Style

Fabio Penna; Andrea Camperi; Maurizio Muscaritoli; Nicoletta Filigheddu; Paola Costelli. 2017. "The role of vitamin D in cancer cachexia." Current Opinion in Supportive & Palliative Care 11, no. 4: 287-292.

Tissue specific stem cells
Published: 24 April 2017 in STEM CELLS
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Muscle regeneration depends on satellite cells (SCs), quiescent precursors that, in consequence of injury or in pathological states such as muscular dystrophies, activate, proliferate, and differentiate to repair the damaged tissue. A subset of SCs undergoes self‐renewal, thus preserving the SC pool and its regenerative potential. Unacylated ghrelin (UnAG) is a circulating hormone that protects muscle from atrophy, promotes myoblast differentiation, and enhances ischemia‐induced muscle regeneration. Here we show that UnAG increases SC activity and stimulates Par polarity complex/p38‐mediated asymmetric division, fostering both SC self‐renewal and myoblast differentiation. Because of those activities on different steps of muscle regeneration, we hypothesized a beneficial effect of UnAG in mdx dystrophic mice, in which the absence of dystrophin leads to chronic muscle degeneration, defective muscle regeneration, fibrosis, and, at later stages of the pathology, SC pool exhaustion. Upregulation of UnAG levels in mdx mice reduces muscle degeneration, improves muscle function, and increases dystrophin‐null SC self‐renewal, maintaining the SC pool. Our results suggest that UnAG has significant therapeutic potential for preserving the muscles in dystrophies. Stem Cells 2017;35:1733–1746

ACS Style

Simone Reano; Elia Angelino; Michele Ferrara; Valeria Malacarne; Hana Sustova; Omar Sabry; Emanuela Agosti; Sara Clerici; Giulia Ruozi; Lorena Zentilin; Flavia Prodam; Stefano Geuna; Mauro Giacca; Andrea Graziani; Nicoletta Filigheddu. Unacylated Ghrelin Enhances Satellite Cell Function and Relieves the Dystrophic Phenotype in Duchenne Muscular Dystrophy mdx Model. STEM CELLS 2017, 35, 1733 -1746.

AMA Style

Simone Reano, Elia Angelino, Michele Ferrara, Valeria Malacarne, Hana Sustova, Omar Sabry, Emanuela Agosti, Sara Clerici, Giulia Ruozi, Lorena Zentilin, Flavia Prodam, Stefano Geuna, Mauro Giacca, Andrea Graziani, Nicoletta Filigheddu. Unacylated Ghrelin Enhances Satellite Cell Function and Relieves the Dystrophic Phenotype in Duchenne Muscular Dystrophy mdx Model. STEM CELLS. 2017; 35 (7):1733-1746.

Chicago/Turabian Style

Simone Reano; Elia Angelino; Michele Ferrara; Valeria Malacarne; Hana Sustova; Omar Sabry; Emanuela Agosti; Sara Clerici; Giulia Ruozi; Lorena Zentilin; Flavia Prodam; Stefano Geuna; Mauro Giacca; Andrea Graziani; Nicoletta Filigheddu. 2017. "Unacylated Ghrelin Enhances Satellite Cell Function and Relieves the Dystrophic Phenotype in Duchenne Muscular Dystrophy mdx Model." STEM CELLS 35, no. 7: 1733-1746.

Journal article
Published: 28 January 2016 in Diabetes
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Excess reactive oxygen species (ROS) generation and inflammation may contribute to obesity-associated skeletal muscle insulin resistance. Ghrelin is a gastric hormone whose unacylated (UnAG) form is associated with whole-body insulin sensitivity in humans and may reduce oxidative stress in non-muscle cells in-vitro. We hypothesized that UnAG 1) lowers muscle ROS production and inflammation and enhances tissue insulin action in lean rats; 2) prevents muscle metabolic alterations and normalizes insulin resistance and hyperglycemia in high-fat diet (HFD)-induced obesity. In 12-week-old lean rats, UnAG (4-day, twice-daily subcutaneous 200µg-injections) reduced gastrocnemius mitochondrial ROS generation and inflammatory cytokines while enhancing AKT-dependent signaling and insulin-stimulated glucose uptake. In HFD-treated mice, chronic UnAG overexpression prevented obesity-associated hyperglycemia and whole-body insulin resistance (insulin-tolerance test), as well as muscle oxidative stress, inflammation and altered insulin signalling. In myotubes, UnAG consistently lowered mitochondrial ROS production and enhanced insulin signalling, while UnAG effects were prevented by siRNA-mediated silencing of the autophagy mediator ATG5. Thus, UnAG lowers mitochondrial ROS production and inflammation while enhancing insulin action in rodent skeletal muscle. In HFD-induced obesity, these effects prevent hyperglycemia and insulin resistance. Stimulated muscle autophagy could contribute to UnAG activities. These findings support UnAG as a therapeutic strategy for obesity-associated metabolic alterations.

ACS Style

Gianluca Gortan Cappellari; Michela Zanetti; Annamaria Semolic; Pierandrea Vinci; Giulia Ruozi; Antonella Falcione; Nicoletta Filigheddu; Gianfranco Guarnieri; Andrea Graziani; Mauro Giacca; Rocco Barazzoni. Unacylated Ghrelin Reduces Skeletal Muscle Reactive Oxygen Species Generation and Inflammation and Prevents High-Fat Diet–Induced Hyperglycemia and Whole-Body Insulin Resistance in Rodents. Diabetes 2016, 65, 874 -886.

AMA Style

Gianluca Gortan Cappellari, Michela Zanetti, Annamaria Semolic, Pierandrea Vinci, Giulia Ruozi, Antonella Falcione, Nicoletta Filigheddu, Gianfranco Guarnieri, Andrea Graziani, Mauro Giacca, Rocco Barazzoni. Unacylated Ghrelin Reduces Skeletal Muscle Reactive Oxygen Species Generation and Inflammation and Prevents High-Fat Diet–Induced Hyperglycemia and Whole-Body Insulin Resistance in Rodents. Diabetes. 2016; 65 (4):874-886.

Chicago/Turabian Style

Gianluca Gortan Cappellari; Michela Zanetti; Annamaria Semolic; Pierandrea Vinci; Giulia Ruozi; Antonella Falcione; Nicoletta Filigheddu; Gianfranco Guarnieri; Andrea Graziani; Mauro Giacca; Rocco Barazzoni. 2016. "Unacylated Ghrelin Reduces Skeletal Muscle Reactive Oxygen Species Generation and Inflammation and Prevents High-Fat Diet–Induced Hyperglycemia and Whole-Body Insulin Resistance in Rodents." Diabetes 65, no. 4: 874-886.

Journal article
Published: 01 December 2015 in Clinical Nutrition Experimental
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Changes in liver mitochondrial function with more oxidized redox state and enhanced inflammation may contribute to the onset of obesity- and insulin resistance-associated hepatic complications, including non-alcoholic fatty liver disease and steato-hepatitis. Unacylated ghrelin (UnAG) is a gastric hormone reported to be associated with lower oxidative stress in different cell types, but its potential effects on liver mitochondrial function, redox state and inflammation in vivo remains undetermined. We investigated the impact of chronic UnAG overexpression (Tg Myh6/Ghrl) leading to systemic upregulation of circulating hormone on mitochondrial ATP production, redox state (oxidized-to-total glutathione) and inflammation markers in lean mice. Compared to wild-type animals (wt), Tg Myh6/Ghrl had superimposable liver weight, triglyceride content and plasma lipid profile. Liver mitochondrial enzyme activities and ATP production as well as oxidized-to-total glutathione were also similar in the two groups. In addition, no differences were observed in tissue inflammation marker TNF-alpha between wild-type and Tg Myh6/Ghrl animals. Thus, chronic systemic UnAG upregulation does not alter liver triglyceride content, mitochondrial function, redox state and inflammation markers in lean mice. These findings do not support a major role of UnAG as a physiological modulator of in vivo liver oxidative-lipid metabolism and inflammation.

ACS Style

Gianluca Gortan Cappellari; Michela Zanetti; Annamaria Semolic; Pierandrea Vinci; Giulia Ruozi; Margherita De Nardo; Nicoletta Filigheddu; Gianfranco Guarnieri; Mauro Giacca; Andrea Graziani; Rocco Barazzoni. Unacylated ghrelin does not alter mitochondrial function, redox state and triglyceride content in rat liver in vivo. Clinical Nutrition Experimental 2015, 4, 1 -7.

AMA Style

Gianluca Gortan Cappellari, Michela Zanetti, Annamaria Semolic, Pierandrea Vinci, Giulia Ruozi, Margherita De Nardo, Nicoletta Filigheddu, Gianfranco Guarnieri, Mauro Giacca, Andrea Graziani, Rocco Barazzoni. Unacylated ghrelin does not alter mitochondrial function, redox state and triglyceride content in rat liver in vivo. Clinical Nutrition Experimental. 2015; 4 ():1-7.

Chicago/Turabian Style

Gianluca Gortan Cappellari; Michela Zanetti; Annamaria Semolic; Pierandrea Vinci; Giulia Ruozi; Margherita De Nardo; Nicoletta Filigheddu; Gianfranco Guarnieri; Mauro Giacca; Andrea Graziani; Rocco Barazzoni. 2015. "Unacylated ghrelin does not alter mitochondrial function, redox state and triglyceride content in rat liver in vivo." Clinical Nutrition Experimental 4, no. : 1-7.

Correction
Published: 23 October 2015 in PLOS ONE
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ACS Style

Francesca Oltolina; Andrea Zamperone; Donato Colangelo; Luca Gregoletto; Simone Reano; Stefano Pietronave; Simone Merlin; Maria Talmon; Eugenio Novelli; Marco Diena; Carmine Nicoletti; Antonio Musarò; Nicoletta Filigheddu; Antonia Follenzi; Maria Prat. Correction: Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential. PLOS ONE 2015, 10, e0141632 .

AMA Style

Francesca Oltolina, Andrea Zamperone, Donato Colangelo, Luca Gregoletto, Simone Reano, Stefano Pietronave, Simone Merlin, Maria Talmon, Eugenio Novelli, Marco Diena, Carmine Nicoletti, Antonio Musarò, Nicoletta Filigheddu, Antonia Follenzi, Maria Prat. Correction: Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential. PLOS ONE. 2015; 10 (10):e0141632.

Chicago/Turabian Style

Francesca Oltolina; Andrea Zamperone; Donato Colangelo; Luca Gregoletto; Simone Reano; Stefano Pietronave; Simone Merlin; Maria Talmon; Eugenio Novelli; Marco Diena; Carmine Nicoletti; Antonio Musarò; Nicoletta Filigheddu; Antonia Follenzi; Maria Prat. 2015. "Correction: Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential." PLOS ONE 10, no. 10: e0141632.

Research article
Published: 16 September 2015 in PLoS ONE
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A major obstacle to an effective myocardium stem cell therapy has always been the delivery and survival of implanted stem cells in the heart. Better engraftment can be achieved if cells are administered as cell aggregates, which maintain their extra-cellular matrix (ECM). We have generated spheroid aggregates in less than 24 h by seeding human cardiac progenitor cells (hCPCs) onto methylcellulose hydrogel-coated microwells. Cells within spheroids maintained the expression of stemness/mesenchymal and ECM markers, growth factors and their cognate receptors, cardiac commitment factors, and metalloproteases, as detected by immunofluorescence, q-RT-PCR and immunoarray, and expressed a higher, but regulated, telomerase activity. Compared to cells in monolayers, 3D spheroids secreted also bFGF and showed MMP2 activity. When spheroids were seeded on culture plates, the cells quickly migrated, displaying an increased wound healing ability with or without pharmacological modulation, and reached confluence at a higher rate than cells from conventional monolayers. When spheroids were injected in the heart wall of healthy mice, some cells migrated from the spheroids, engrafted, and remained detectable for at least 1 week after transplantation, while, when the same amount of cells was injected as suspension, no cells were detectable three days after injection. Cells from spheroids displayed the same engraftment capability when they were injected in cardiotoxin-injured myocardium. Our study shows that spherical in vivo ready-to-implant scaffold-less aggregates of hCPCs able to engraft also in the hostile environment of an injured myocardium can be produced with an economic, easy and fast protocol.

ACS Style

Francesca Oltolina; Andrea Zamperone; Donato Colangelo; Luca Gregoletto; Simone Reano; Stefano Pietronave; Simone Merlin; Maria Talmon; Eugenio Novelli; Marco Diena; Carmine Nicoletti; Antonio Musarò; Nicoletta Filigheddu; Antonia Follenzi; Maria Prat. Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential. PLoS ONE 2015, 10, e0137999 .

AMA Style

Francesca Oltolina, Andrea Zamperone, Donato Colangelo, Luca Gregoletto, Simone Reano, Stefano Pietronave, Simone Merlin, Maria Talmon, Eugenio Novelli, Marco Diena, Carmine Nicoletti, Antonio Musarò, Nicoletta Filigheddu, Antonia Follenzi, Maria Prat. Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential. PLoS ONE. 2015; 10 (9):e0137999.

Chicago/Turabian Style

Francesca Oltolina; Andrea Zamperone; Donato Colangelo; Luca Gregoletto; Simone Reano; Stefano Pietronave; Simone Merlin; Maria Talmon; Eugenio Novelli; Marco Diena; Carmine Nicoletti; Antonio Musarò; Nicoletta Filigheddu; Antonia Follenzi; Maria Prat. 2015. "Human Cardiac Progenitor Spheroids Exhibit Enhanced Engraftment Potential." PLoS ONE 10, no. 9: e0137999.

Journal article
Published: 11 June 2015 in Nature Communications
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Functional screening of expression libraries in vivo would offer the possibility of identifying novel biotherapeutics without a priori knowledge of their biochemical function. Here we describe a procedure for the functional selection of tissue-protective factors based on the in vivo delivery of arrayed cDNA libraries from the mouse secretome using adeno-associated virus (AAV) vectors. Application of this technique, which we call FunSel, in the context of acute ischaemia, revealed that the peptide ghrelin protects skeletal muscle and heart from ischaemic damage. When delivered to the heart using an AAV9 vector, ghrelin markedly reduces infarct size and preserves cardiac function over time. This protective activity associates with the capacity of ghrelin to sustain autophagy and remove dysfunctional mitochondria after myocardial infarction. Our findings describe an innovative tool to identify biological therapeutics and reveal a novel role of ghrelin as an inducer of myoprotective autophagy.

ACS Style

Giulia Ruozi; Francesca Bortolotti; Antonella Falcione; Matteo Dal Ferro; Laura Ukovich; Antero Macedo; Lorena Zentilin; Nicoletta Filigheddu; Gianluca Gortan Cappellari; Giovanna Baldini; Marina Zweyer; Rocco Barazzoni; Andrea Graziani; Serena Zacchigna; Mauro Giacca. AAV-mediated in vivo functional selection of tissue-protective factors against ischaemia. Nature Communications 2015, 6, 7388 .

AMA Style

Giulia Ruozi, Francesca Bortolotti, Antonella Falcione, Matteo Dal Ferro, Laura Ukovich, Antero Macedo, Lorena Zentilin, Nicoletta Filigheddu, Gianluca Gortan Cappellari, Giovanna Baldini, Marina Zweyer, Rocco Barazzoni, Andrea Graziani, Serena Zacchigna, Mauro Giacca. AAV-mediated in vivo functional selection of tissue-protective factors against ischaemia. Nature Communications. 2015; 6 (1):7388.

Chicago/Turabian Style

Giulia Ruozi; Francesca Bortolotti; Antonella Falcione; Matteo Dal Ferro; Laura Ukovich; Antero Macedo; Lorena Zentilin; Nicoletta Filigheddu; Gianluca Gortan Cappellari; Giovanna Baldini; Marina Zweyer; Rocco Barazzoni; Andrea Graziani; Serena Zacchigna; Mauro Giacca. 2015. "AAV-mediated in vivo functional selection of tissue-protective factors against ischaemia." Nature Communications 6, no. 1: 7388.

Review article
Published: 16 April 2015 in International Journal of Endocrinology
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Fibrosis can affect almost all tissues and organs, it often represents the terminal stage of chronic diseases, and it is regarded as a major health issue for which efficient therapies are needed. Tissue injury, by inducing necrosis/apoptosis, triggers inflammatory response that, in turn, promotes fibroblast activation and pathological deposition of extracellular matrix. Acylated and unacylated ghrelin are the main products of the ghrelin gene. The acylated form, through its receptor GHSR-1a, stimulates appetite and growth hormone (GH) release. Although unacylated ghrelin does not bind or activate GHSR-1a, it shares with the acylated form several biological activities. Ghrelin peptides exhibit anti-inflammatory, antioxidative, and antiapoptotic activities, suggesting that they might represent an efficient approach to prevent or reduce fibrosis. The aim of this review is to summarize the available evidence regarding the effects of acylated and unacylated ghrelin on different pathologies and experimental models in which fibrosis is a predominant characteristic.

ACS Style

Elia Angelino; Simone Reano; Michele Ferrara; Emanuela Agosti; Andrea Graziani; Nicoletta Filigheddu. Antifibrotic Activity of Acylated and Unacylated Ghrelin. International Journal of Endocrinology 2015, 2015, 1 -9.

AMA Style

Elia Angelino, Simone Reano, Michele Ferrara, Emanuela Agosti, Andrea Graziani, Nicoletta Filigheddu. Antifibrotic Activity of Acylated and Unacylated Ghrelin. International Journal of Endocrinology. 2015; 2015 ():1-9.

Chicago/Turabian Style

Elia Angelino; Simone Reano; Michele Ferrara; Emanuela Agosti; Andrea Graziani; Nicoletta Filigheddu. 2015. "Antifibrotic Activity of Acylated and Unacylated Ghrelin." International Journal of Endocrinology 2015, no. : 1-9.