Core Viewpoint - The research highlights the critical role of the epigenetic regulator BAZ2B in hepatic senescence and metabolic dysfunction-associated steatohepatitis (MASH) fibrosis, providing a theoretical foundation for developing new therapeutic strategies [2][4][7]. Group 1: Research Findings - The study reveals an epigenetic mechanism linking liver aging to MASH fibrosis, with the upregulation of chromatin remodeler BAZ2B associated with MASH pathology in certain liver cells [4]. - In mouse models, gene knockout or liver cell-specific knockdown of Baz2b alleviates hepatic senescence and MASH fibrosis by maintaining PPARα-mediated lipid metabolism, which is impaired in naturally aged and MASH mice [4][5]. - BAZ2B directly binds to the promoter regions of genes related to the PPARα signaling pathway, reducing chromatin accessibility and downregulating gene expression [5]. Group 2: Implications - The BAZ2B-PPARα-lipid metabolism signaling axis is identified as a crucial link in the progression from liver aging to MASH fibrosis, suggesting that BAZ2B may serve as a potential therapeutic target for liver aging and fibrosis [7].