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TGF beta, smooth muscle cells and coronary artery disease: a review

机译:TGFβ,平滑肌细胞和冠状动脉疾病:综述

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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 (TGF beta), its receptors and downstream signalling proteins have demonstrated the importance of this pleiotropic cytokine during vasculogenesis and in the maintenance of vascular homeostasis. Dysregulated TGF beta 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 TGF beta signalling in SMCs, highlighting the ways in which this multifaceted cytokine regulates SMC behaviour and phenotype in cardiovascular diseases driven by intimal hyperplasia.
机译:过量的血管平滑肌细胞(SMC)增殖,迁移和细胞外基质(ECM)合成是内膜增生的关键事件,对血管损伤的急性或慢性源的病理生理反应,这可能导致血管腔的闭塞狭窄。动脉粥样硬化,冠状动脉疾病的主要原因,其特征在于慢性血管炎症和血脂血症,而血管内血液抑制等冠状动脉抵抗和旁路接枝等血管损伤代表急性形式的血管损伤。转化生长因子-β(TGFβ)的基因敲除,其受体和下游信号蛋白已经证明了这种血管生成期间这种抗血液细胞因子的重要性和维持血管稳态。 DysroguredTGFβ信号传导是许多血管疾病的标志,并且已经与病理血管细胞表型,纤维化和ECM重塑的诱导有关。在这里,我们概述了SMC中的TGFβ信令,突出了这种多方型细胞因子调节Intrimal增生驱动的心血管疾病中SMC行为和表型的方式。

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