ArticleJournal of cachexia, sarcopenia and muscle2025
Skeletal Muscle PGC-1α Remodels Mitochondrial Phospholipidome but Does Not Alter Energy Efficiency for ATP Synthesis.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pathophysiological mechanisms of post-exertional malaise: an integrative analysis based on the metabolism-immune-neuro interaction model.Frontiers in immunology · 2026Pooled it
- Metabolic Overdrive in Elite Sport: A Systems Model of AMPK-mTOR Oscillation, NADInternational journal of molecular sciences · 2026Review
- Skeletal Muscle PGC-1α Remodels Mitochondrial Phospholipidome but Does Not Alter Energy Efficiency for ATP Synthesis.Journal of cachexia, sarcopenia and muscle · 2025Article
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Abstract
backgroundThe coupling of oxygen consumption to ATP synthesis via oxidative phosphorylation (OXPHOS) is central for cellular energy homeostasis. Some studies suggest exercise training increases the efficiency of ATP synthesis, but the molecular mechanisms are unclear. We have previously shown that exercise remodels the lipid composition of mitochondrial membranes, and some of these changes in mitochondrial lipids might influence OXPHOS efficiency (ATP produced per O
methodsMice with skeletal muscle-specific overexpression of PGC-1α (MCK-PGC-1α) and their wildtype littermates were used for this study. Lipid mass spectrometry and quantitative PCR were used to assess muscle mitochondrial lipid composition and their biosynthesis pathway. The abundance of OXPHOS enzymes was determined by Western blotting. High-resolution respirometry and fluorometry analyses were performed to characterize mitochondrial bioenergetics (ATP production, O
resultsLipidomic analyses of skeletal muscle mitochondria from wildtype and MCK-PGC-1α mice revealed that PGC-1α increases the concentrations of cone-shaped lipids such as phosphatidylethanolamine (PE; +25%, p < 0.0001), cardiolipin (CL; +184%, p < 0.0001) and lysophospholipids (+34%-94%, all p < 0.01), while decreasing the concentrations of phosphatidylcholine (PC; -4%, p = 0.0020), phosphatidylinositol (PI; -17%, p < 0.0001) and phosphatidic acid (PA; -35%, p < 0.0001). However, while PGC-1α overexpression increased the abundance of OXPHOS enzymes (two- to fourfold, p < 0.0001), the rate of O
conclusionsCollectively, overexpression of PGC-1α promotes the biosynthesis of mitochondrial PE and CL, but neither PGC-1α nor the mitochondrial membrane lipid remodelling induced in MCK-PGC-1α mice is sufficient to increase the efficiency of mitochondrial ATP synthesis. These findings indicate that PGC-1α-dependent mechanisms or changes in mitochondrial membrane lipids may be insufficient to alter P/O. While muscles from MCK-PGC-1α mice are known not to completely phenocopy adaptations with exercise training, our findings also highlight that there is a need to examine whether exercise training indeed improves P/O in mouse skeletal muscle.
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