Histone lactylation-mediated metabolic remodeling in vascular smooth muscle cells aggravates aortic aneurysm and dissection via promoting lactate accumulation

The phenotypic switch of vascular smooth muscle cells (VSMCs) is a crucial pathogenesis in aortic aneurysm and dissection (AAD), metabolic remodeling from oxidative phosphorylation (OXPHOS) to glycolysis involved in the process. Histone lactylation expression was analyzed in aorta of aortic aneurysm (AA) patients and AAD mice, as well as the AngII(angiotensin II)-treated VSMCs. CUT&Tag was used to explore the downstream target gene for H4K16 lactylation (H4K16la) between AngII-induced VSMCs and Control. The finding was to explore the impact of histone lactylation (H4K16la) on the progress of AAD. Overall design: CUT&Tag analysis of H4K16 lactylation in human aortic vascular smooth muscle cells.