ArticleNature communications2023
Linker histone variant H1.2 is a brake on white adipose tissue browning.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Hepatic GAPDH prevents excessive fasting-induced steatosis via serine-dependent inhibition of diacylglycerol synthesis.Cell death and differentiation · 2026Article
- Neofunctionalization of H1 linker histones drives divergent gene expression and histone methylation in Cryptococcus neoformans.Communications biology · 2026Article
- Latest Advances in Obesity Treatment by Regulating Adipocyte Thermogenesis.PPAR research · 2026Review
- From endocrine to immune: therapeutic potential of brown adipose tissue in remodelling the cardiovascular immune microenvironment.Frontiers in immunology · 2026Review
- The multifaceted regulation of white adipose tissue browning and their therapeutic potential.Journal of physiology and biochemistry · 2025Review
- Adipocyte CLDN5 promotes thermogenesis and energy expenditure through regulation of IL10 expression.Nature communications · 2025Article
- ISG15 Enhances the Activity of γ-Glutamate Cysteine Ligase to Suppress Apoptosis in High Fat Diet-Promoted Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phase Separation of Chromatin Structure-related Biomolecules: A Driving Force for Epigenetic Regulations.Current protein & peptide science · 2024Review
- An antioxidant feedforward cycle coordinated by linker histone variant H1.2 and NRF2 that drives nonsmall cell lung cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Tet1 deficiency exacerbates oxidative stress in acute kidney injury by regulating superoxide dismutase.Theranostics · 2023Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipose-tissue is a central metabolic organ for whole-body energy homeostasis. Here, we find that highly expressed H1.2, a linker histone variant, senses thermogenic stimuli in beige and brown adipocytes. Adipocyte H1.2 regulates thermogenic genes in inguinal white-adipose-tissue (iWAT) and affects energy expenditure. Adipocyte H1.2 deletion (H1.2AKO) male mice show promoted iWAT browning and improved cold tolerance; while overexpressing H1.2 shows opposite effects. Mechanistically, H1.2 binds to the promoter of Il10rα, which encodes an Il10 receptor, and positively regulates its expression to suppress thermogenesis in a beige cell autonomous manner. Il10rα overexpression in iWAT negates cold-enhanced browning of H1.2AKO male mice. Increased H1.2 level is also found in WAT of obese humans and male mice. H1.2AKO male mice show alleviated fat accumulation and glucose intolerance in long-term normal chow-fed and high fat diet-fed conditions; while Il10rα overexpression abolishes these effects. Here, we show a metabolic function of H1.2-Il10rα axis in iWAT.
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