ReviewFrontiers in endocrinology2026
Intramyocellular lipid droplet-mitochondria uncoupling drives muscle atrophy via metabolite-directed epigenetic reprogramming: a review.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Type 2 diabetes mellitus (T2DM)-associated sarcopenia is driven by protein degradation and impaired myogenic regeneration. While classical models emphasize cytosolic kinase pathways, the subcellular mechanisms mediating lipotoxicity-induced chronic catabolism remain incompletely understood. This review elucidates a tripartite pathological cascade comprising organelle structural uncoupling, metabolic intermediate overflow, and epigenetic reprogramming. Chronic intramyocellular lipid accumulation disrupts lipid droplet-mitochondria contact (LDMC) sites, largely via Mfn2 modification. This spatial dissociation impairs mitochondrial oxidation, driving the nucleocytoplasmic accumulation of polar metabolites, specifically Acetyl-CoA, succinate, and lactate. Acting as covalent substrates or competitive inhibitors, these metabolites modulate histone-modifying enzymes such as p300/CBP and JmjC-domain demethylases. Consequently, this substrate-driven epigenetic remodeling increases chromatin accessibility at E3 ubiquitin ligase promoters (
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