ArticleCell metabolism2025
RBM43 controls PGC1α translation and a PGC1α-STING signaling axis.
Article in Cell metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- TUFT1 stabilizes TGF-β receptor II protein and facilitates activation of hepatic stellate cells into metastasis-promoting myofibroblasts.Cell death and differentiation · 2026Article
- CTRP3 alleviates neuropathic pain by improving mitochondrial biogenesis and mitochondrial unfolded protein response via spinal SIRT1 in rats.International journal of molecular medicine · 2026Article
- From energy metabolic homeostasis to immune remodeling: the role and therapeutic potential of STING signaling in the tumor microenvironment.Cell communication and signaling : CCS · 2026Review
- Bioactive Constituents and Therapeutic Mechanisms of Shenfu Decoction in a Rat Model of Seawater-Immersion-Induced Accidental Hypothermia.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Fatty acid oxidation drives acetyl-CoA-dependent H3K9ac reprogramming to promote adaptive resistance to BRAFCell death & disease · 2026Article
- Mitophagy and oxidative stress in chronic kidney disease (Review).Molecular medicine reports · 2026Review
- Roles of RNA-binding proteins in macrophage function regulation and immunotherapy.Frontiers in cell and developmental biology · 2026Review
- The role of exercise-mediated mitochondrial quality control remodeling in aging.Frontiers in cell and developmental biology · 2026Review
- Effects of different sugar-lipid ratio diets on the occurrence of type 2 diabetes mellitus.Frontiers in endocrinology · 2026Article
- Role of the cGAS-STING signaling pathway in diabetes mellitus and its complications: from mechanisms to therapeutics.Frontiers in pharmacology · 2026Review
- β-Hydroxybutyrate-induced mitochondrial dysfunction and oxidative stress in BMSCs are ameliorated by mitophagy activation.Frontiers in cell and developmental biology · 2026Article
- Analyzing the potential targets and mechanism of per- and polyfluoroalkyl substances (PFAS) on breast cancer by integrating network toxicology, single-cell sequencing, spatial transcriptomics, and molecular simulation.Functional & integrative genomics · 2025Article
- Peptide YY fragment PYY1-36 disrupts mitochondrial biogenesis via RBM43-dependent PGC-1α translation inhibition.Investigational new drugs · 2025Article
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6 authors.
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Abstract
Obesity is associated with systemic inflammation that impairs mitochondrial function. This disruption curtails oxidative metabolism, limiting adipocyte lipid metabolism and thermogenesis, a metabolically beneficial program that dissipates chemical energy as heat. Here, we show that PGC1α, a key governor of mitochondrial biogenesis, is negatively regulated at the level of its mRNA translation by the RNA-binding protein RBM43. RBM43 is induced by inflammatory cytokines and suppresses mitochondrial biogenesis in a PGC1α-dependent manner. In mice, adipocyte-selective Rbm43 disruption elevates PGC1α translation and oxidative metabolism. In obesity, Rbm43 loss improves glucose tolerance, reduces adipose inflammation, and suppresses activation of the innate immune sensor cGAS-STING in adipocytes. We further identify a role for PGC1α in safeguarding against cytoplasmic accumulation of mitochondrial DNA, a cGAS ligand. The action of RBM43 defines a translational regulatory axis by which inflammatory signals dictate cellular energy metabolism and contribute to metabolic disease pathogenesis.
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