ArticleScience advances2024
Succinate dehydrogenase-complex II regulates skeletal muscle cellular respiration and contractility but not muscle mass in genetically induced pulmonary emphysema.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Long-term DNA methylation changes induced by age and elevated COSkeletal muscle · 2025Article
- Chronic succinate exposure does not cause liver injury.American journal of physiology. Endocrinology and metabolism · 2025Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Voluntary Exercise-Induced Skeletal Muscle Responses in Young and Aged Mice on a High-Fat Diet.Cureus · 2025Article
- Rapamycin improves satellite cells' autophagy and muscle regeneration during hypercapnia.JCI insight · 2025Article
- An in vitro model to study molecular pathogenesis of sarcopenia established by a SASP-dependent human myotube culture.PloS one · 2025Article
- Quantitative Computed Tomography Biomarkers of Emphysema Severity in Chronic Obstructive Pulmonary Disease: Insights from Muscle Mass, Fat Volume, and Vascular Dimensions.Advanced biomedical research · 2025Article
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Authors and funding
16 authors.
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Abstract
Reduced skeletal muscle mass and oxidative capacity coexist in patients with pulmonary emphysema and are independently associated with higher mortality. If reduced cellular respiration contributes to muscle atrophy in that setting remains unknown. Using a mouse with genetically induced pulmonary emphysema that recapitulates muscle dysfunction, we found that reduced activity of succinate dehydrogenase (SDH) is a hallmark of its myopathic changes. We generated an inducible, muscle-specific SDH knockout mouse that demonstrates lower mitochondrial oxygen consumption, myofiber contractility, and exercise endurance. Respirometry analyses show that in vitro complex I respiration is unaffected by loss of SDH subunit C in muscle mitochondria, which is consistent with the pulmonary emphysema animal data. SDH knockout initially causes succinate accumulation associated with a down-regulated transcriptome but modest proteome effects. Muscle mass, myofiber type composition, and overall body mass constituents remain unaltered in the transgenic mice. Thus, while SDH regulates myofiber respiration in experimental pulmonary emphysema, it does not control muscle mass or other body constituents.
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