Excessive vascular smooth muscle cell (SMC) proliferation, migration and extracellular matrix (ECM) synthesis are key events in the development of intimal hyperplasia, a pathophysiological response to acute or chronic sources of vascular damage that can lead to occlusive narrowing of the vessel lumen. Atherosclerosis, the primary cause of coronary artery disease, is characterised by chronic vascular inflammation and dyslipidemia, while revascularisation surgeries such as coronary stenting and bypass grafting represent acute forms of vascular injury. Gene knockouts of transforming growth factor-beta (TGFβ), its receptors and downstream signalling proteins have demonstrated the importance of this pleiotropic cytokine during vasculogenesis and in the maintenance of vascular homeostasis. Dysregulated TGFβ signalling is a hallmark of many vascular diseases, and has been associated with the induction of pathological vascular cell phenotypes, fibrosis and ECM remodelling. Here we present an overview of TGFβ signalling in SMCs, highlighting the ways in which this multifaceted cytokine regulates SMC behaviour and phenotype in cardiovascular diseases driven by intimal hyperplasia.

中文翻译：

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TGFβ、平滑肌细胞和冠状动脉疾病：综述。


血管平滑肌细胞（SMC）过度增殖、迁移和细胞外基质（ECM）合成是内膜增生发生的关键事件，内膜增生是对急性或慢性血管损伤的病理生理反应，可导致血管腔闭塞性狭窄。动脉粥样硬化是冠状动脉疾病的主要原因，其特征是慢性血管炎症和血脂异常，而冠状动脉支架置入术和旁路移植术等血运重建手术则代表急性形式的血管损伤。转化生长因子-β (TGFβ)、其受体和下游信号蛋白的基因敲除证明了这种多效性细胞因子在血管生成和维持血管稳态过程中的重要性。 TGFβ 信号传导失调是许多血管疾病的标志，并且与病理性血管细胞表型、纤维化和 ECM 重塑的诱导有关。在这里，我们概述了 SMC 中的 TGFβ 信号传导，强调了这种多方面的细胞因子在由内膜增生驱动的心血管疾病中调节 SMC 行为和表型的方式。