Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is one of the most common causes of liver dysfunction worldwide, posing a significant economic burden. However, our understanding of the cellular and molecular mechanisms underlyi...

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Main Authors: Irfana Zahoor, Gh Jeelani Mir, Nazir Ahmad Lone, Nissar Ul Ashraf
Format: Article
Language:English
Published: Korean Society for the Study of Obesity 2025-07-01
Series:Journal of Obesity & Metabolic Syndrome
Subjects:
Online Access:http://www.jomes.org/journal/view.html?doi=10.7570/jomes24041
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author Irfana Zahoor
Gh Jeelani Mir
Nazir Ahmad Lone
Nissar Ul Ashraf
author_facet Irfana Zahoor
Gh Jeelani Mir
Nazir Ahmad Lone
Nissar Ul Ashraf
author_sort Irfana Zahoor
collection DOAJ
description Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is one of the most common causes of liver dysfunction worldwide, posing a significant economic burden. However, our understanding of the cellular and molecular mechanisms underlying the pathogenesis of MASLD is in its early stages. Over the last two decades, epigenetic mechanisms and autophagy have emerged as two independent phenomena that control cellular and molecular processes in health and disease. Epigenetic events and defects in autophagy have been linked with the pathogenesis of MASLD and metabolic dysfunction-associated steatohepatitis (MASH) in cellular studies, mouse models, and human research. However, the connection between epigenetic mechanisms and autophagy regulation in MASLD and MASH pathogenesis remains unclear. This review highlights the importance of epigenetic modifications and their regulatory switches in controlling downstream pathways that significantly impact metabolic disease pathogenesis. We also review the need to identify key epigenetic factors regulating autophagy in MASLD and MASH pathogenesis. Such insights could aid the development of novel strategies to restore autophagy and improve disease outcomes.
format Article
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institution DOAJ
issn 2508-6235
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publishDate 2025-07-01
publisher Korean Society for the Study of Obesity
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series Journal of Obesity & Metabolic Syndrome
spelling doaj-art-6b244487019c402496af3cbfa5ef54742025-08-20T02:46:06ZengKorean Society for the Study of ObesityJournal of Obesity & Metabolic Syndrome2508-62352025-07-0134325326710.7570/jomes24041jomes24041Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver DiseaseIrfana Zahoor0Gh Jeelani Mir1Nazir Ahmad Lone2Nissar Ul Ashraf3Departmemt of Biochemistry, Government College for Women, Nawakadal Srinagar, Jammu & Kashmir, IndiaDepartment of Clinical Biochemistry, Government Degree College Sopore, Jammu & Kashmir, IndiaDepartment of Biotechnology, Government College for Women, Nawakadal Srinagar, Jammu & Kashmir, IndiaDepartmemt of Biochemistry, Government College for Women, Nawakadal Srinagar, Jammu & Kashmir, IndiaMetabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, is one of the most common causes of liver dysfunction worldwide, posing a significant economic burden. However, our understanding of the cellular and molecular mechanisms underlying the pathogenesis of MASLD is in its early stages. Over the last two decades, epigenetic mechanisms and autophagy have emerged as two independent phenomena that control cellular and molecular processes in health and disease. Epigenetic events and defects in autophagy have been linked with the pathogenesis of MASLD and metabolic dysfunction-associated steatohepatitis (MASH) in cellular studies, mouse models, and human research. However, the connection between epigenetic mechanisms and autophagy regulation in MASLD and MASH pathogenesis remains unclear. This review highlights the importance of epigenetic modifications and their regulatory switches in controlling downstream pathways that significantly impact metabolic disease pathogenesis. We also review the need to identify key epigenetic factors regulating autophagy in MASLD and MASH pathogenesis. Such insights could aid the development of novel strategies to restore autophagy and improve disease outcomes.http://www.jomes.org/journal/view.html?doi=10.7570/jomes24041metabolic dysfunction-associated steatotic liver diseasemetabolic dysfunction-associated steatohepatitisautophagychromatindna methylationhistone methylationhistone acetylation
spellingShingle Irfana Zahoor
Gh Jeelani Mir
Nazir Ahmad Lone
Nissar Ul Ashraf
Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
Journal of Obesity & Metabolic Syndrome
metabolic dysfunction-associated steatotic liver disease
metabolic dysfunction-associated steatohepatitis
autophagy
chromatin
dna methylation
histone methylation
histone acetylation
title Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
title_full Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
title_fullStr Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
title_full_unstemmed Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
title_short Crosstalk between Epigenetics and Autophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease
title_sort crosstalk between epigenetics and autophagy in metabolic dysfunction associated steatotic liver disease
topic metabolic dysfunction-associated steatotic liver disease
metabolic dysfunction-associated steatohepatitis
autophagy
chromatin
dna methylation
histone methylation
histone acetylation
url http://www.jomes.org/journal/view.html?doi=10.7570/jomes24041
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AT ghjeelanimir crosstalkbetweenepigeneticsandautophagyinmetabolicdysfunctionassociatedsteatoticliverdisease
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AT nissarulashraf crosstalkbetweenepigeneticsandautophagyinmetabolicdysfunctionassociatedsteatoticliverdisease