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

GSE301206 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2026/02/12 Platform GPL24676
Summary
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.
Published in
Histone Lactylation-Mediated Metabolic Remodeling in Vascular Smooth Muscle Cells Aggravates Aortic Aneurysm and Dissection by Promoting Lactate Accumulation
Liu L, Zhang J, Dong Z et al. · Circulation 2026 · PMID 41487086 · doi:10.1161/CIRCULATIONAHA.125.072576
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Also filed as BioProject PRJNA1284268 and SRA study SRP596220. Searching any of these in the dataset finder brings you back here.

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