ArticleActa pharmacologica Sinica2026
Histone methyltransferase G9a drives vascular smooth muscle cell proliferation and intimal hyperplasia in mice.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a critical role in vascular remodeling associated with various cardiovascular disorders. G9a, also known as euchromatic histone methyltransferase 2 (EHMT2), is a lysine methyltransferase that influences histone modifications, particularly H3K9me1 and H3K9me2. In this study we investigated the role of G9a in promoting VSMC proliferation and vascular intimal hyperplasia and the underlying mechanisms. To induce VSMC proliferation, primary aortic VSMCs were treated with platelet-derived growth factor-BB (PDGF-BB) and 10% fetal bovine serum (FBS) in vitro. An in vivo model of carotid intimal hyperplasia was established in mice by ligating the left common carotid artery just below the bifurcation. We showed that the expression levels of G9a were significantly elevated in both in vitro and in vivo models of VSMC proliferation. In the primary aortic VSMCs, co-treatment with G9a inhibitor UNC0642 (1 μM) effectively reduced cell viability, cyclin D1 expression, and EdU incorporation induced by PDGF-BB or 10% FBS. In mouse carotid intimal hyperplasia model, administration of UNC0642 (50 mg·kg
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