BAHCC1 Drives Smooth Muscle Plasticity and Neointima via Epigenetic Repression.

BAHCC1 is upregulated in human restenotic and atherosclerotic arteries and rat arteries with IH, and its H3K27me3 binding supports neointima formation in injury models.

• Why it matters: Vascular smooth muscle cell phenotypic plasticity drives neointimal hyperplasia and atherosclerosis, but how epigenetic reader proteins regulate this transition is unclear.
• What they did: The study used BAHCC1 silencing, SMC-specific deletion, and an H3K27me3-binding-deficient BAHCC1 Y2537A knock-in in human artery samples and rat/mouse arterial injury models, plus transcriptomic/epigenomic profiling and epigenetic editing in human aortic SMCs.
• The result: BAHCC1-dependent repression of the IH suppressor LMO7 via H3K27me3 reading and corepressor recruitment (including SAP30 and RBBP4/7) promotes dedifferentiation and IH, and LMO7 knockdown reverses BAHCC1 effects on human SMC phenotype while worsening IH in BAHCC1 Y2537A mice.

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