ArticleScientific reports2025
Altered mitochondrial unfolded protein response and FGF21 secretion in MASLD progression and the effect of exercise intervention.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Metabolic dysfunction-associated steatotic liver disease: pathogenic mechanisms and exercise-induced molecular adaptations.Lipids in health and disease · 2026Review
- Exercise as a Programmable Regulator of Mitophagy Sensitivity in Aging Muscle and Age-Related Disease.IUBMB life · 2026Review
- Occupational-circadian disruption and physical inactivity conjointly amplify fatty liver risk: based on liver ultrasound transient elastography.International journal of occupational medicine and environmental health · 2026Article
- Exercise-Induced Hepatic Mitochondrial Reprogramming Across Muscle-Gut-Thyroid Axes in MASLD/MASH.International journal of molecular sciences · 2026Review
- Mitochondrial Communication with Cellular Organelles in the Pathogenesis of Fatty Liver Disease in Domestic and Model Animals.Animals : an open access journal from MDPI · 2026Review
- Study on biomarkers of homocysteine-induced transformation of vascular smooth muscle cells into foam cells.Scientific reports · 2026Article
- Natural Product Treatment for Metabolic Dysfunction-Associated Steatotic Liver Disease: Targeted Mitochondrial Quality Control.Drug design, development and therapy · 2026Review
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- UPRmt-regulated mitokines: novel strategies for myocardial injury repair.Frontiers in cell and developmental biology · 2025Review
- Pharmacological and non-pharmacological modulation of endoplasmic reticulum stress in pediatric diabetes.Frontiers in endocrinology · 2025Review
- Restoring metabolic flexibility: targeting organelle interaction networks in the pathogenesis and therapy of MASLD.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
11 authors.
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Abstract
A high-calorie diet and lack of exercise are the most important risk factors contributing to metabolic dysfunction-associated steatotic liver disease (MASLD) initiation and progression. The precise molecular mechanisms of mitochondrial function alteration during MASLD development remain to be fully elucidated. In this study, a total of 60 male C57BL/6J mice were maintained on a normal or amylin liver NASH (AMLN) diet for 6 or 10 weeks. Some of the mice were then subjected to voluntary wheel running, while the other mice were fed a normal or AMLN diet until 14 and 18 weeks. The results showed that hepatic lipid deposition and the PERK-eIF2α-ATF4 pathway were significantly increased with prolonged duration of AMLN diet. However, expression of mitochondrial unfolded protein response (UPRmt) genes and mitokine FGF21 secretion were significantly enhanced in the 14-week AMLN diet mice, but were markedly reduced with the excessive lipid deposition induced by longer AMLN diet. Additionally, the exercise intervention acts as a regulator to optimize UPRmt signal transduction and to enhance mitochondrial homeostasis by improving mitochondrial function, reversing the UPRmt activation pattern, and increasing FGF21 secretion, which plays a pivotal role in delaying the occurrence and development of MASLD.
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