METTL14 inhibits atherogenesis by epigenetically activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs - PubMed
6 hours ago
- #Atherosclerosis
- #Epigenetics
- #Lipid Metabolism
- METTL14 inhibits atherogenesis by activating PPAR-α/γ transcription and fatty acid oxidation in VSMCs.
- VSMC-specific Mettl14 knockout mice showed accelerated foam cell formation and exacerbated atherosclerosis.
- METTL14 regulates phenotypic switching of VSMCs and modulates VSMC-derived macrophage-like cells in plaques.
- METTL14 enhances SETD1A-mediated H3K4 trimethylation to regulate Ppara and Pparg transcription in an m6A-independent manner.
- Activation of PPAR-γ with rosiglitazone restored mitochondrial OXPHOS in Mettl14-deficient VSMCs, reducing lipid accumulation.
- AAV gene therapy recapitulating Mettl14 expression inhibited atherosclerosis progression without liver dysfunction.