ArticleNature metabolism2025
Kdm2a inhibition in skeletal muscle improves metabolic flexibility in obesity.
Article in Nature metabolism, 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.
- Skeletal muscle H3K18 lactylation inhibits hepatic gluconeogenesis through IL-6 mediated interorgan communication.Science advances · 2026Article
- SIRT1 deacetylates PKM2 to constrain lactate production and protect against premature ovarian insufficiency.Life medicine · 2026Article
- The cGAS-STING pathway contributes to cisplatin-induced skeletal muscle atrophy through altered proteostasis and myogenic signaling.Cell communication and signaling : CCS · 2026Article
- MORF4L1 regulation and its role in chromatin remodeling, DNA damage, cellular senescence, and cardiometabolic disease.Vascular pharmacology · 2026Review
- Farnesoid X receptor deficiency accelerates aging and systemic functional decline in male mice.Biogerontology · 2026Article
- Sarcopenia and body temperature-the significance of interorgan metabolic networks in skeletal muscle atrophy.Endocrine journal · 2026Review
- Integrin β3 Orchestrates Hepatic Steatosis via a Novel CD36-Dependent Lipid Uptake Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Ubc9-Mediated SUMOylation of RPL3, an Unappreciated Mechanism against Hepatocyte Senescence by Repressing the DHX9-p16 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Kynurenine-mediated redox regulation provides neuroprotection in central retinal artery occlusion.Journal of translational medicine · 2025Article
- Epigenetic Changes Associated With Obesity-related Metabolic Comorbidities.Journal of the Endocrine Society · 2025Review
- Cardiometabolic disease management: influences from epigenetics.Epigenomics · 2025Review
- Pu-erh tea attenuates obesity by remodeling gut microbiota and activating energy expenditure.Frontiers in microbiology · 2025Article
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Skeletal muscle is a critical organ in maintaining homoeostasis against metabolic stress, and histone post-translational modifications are pivotal in those processes. However, the intricate nature of histone methylation in skeletal muscle and its impact on metabolic homoeostasis have yet to be elucidated. Here, we report that mitochondria-rich slow-twitch myofibers are characterized by significantly higher levels of H3K36me2 along with repressed expression of Kdm2a, an enzyme that specifically catalyses H3K36me2 demethylation. Deletion or inhibition of Kdm2a shifts fuel use from glucose under cold challenge to lipids under obese conditions by increasing the proportion of mitochondria-rich slow-twitch myofibers. This protects mice against cold insults and high-fat-diet-induced obesity and insulin resistance. Mechanistically, Kdm2a deficiency leads to a marked increase in H3K36me2 levels, which then promotes the recruitment of Mrg15 to the Esrrg locus to process its precursor messenger RNA splicing, thereby reshaping skeletal muscle metabolic profiles to induce slow-twitch myofiber transition. Collectively, our data support the role of Kdm2a as a viable target against metabolic stress.
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Registered trials
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