Endoplasmic Reticulum Stress in Arterial Smooth Muscle Cells: A Novel Regulator of Vascular Disease.
Endoplasmic Reticulum Stress in Arterial Smooth Muscle Cells: A Novel Regulator of Vascular Disease.
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DOI：
10.2174/1573403x12666161014094738
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发表时间：
2017
影响因子：
1.9
通讯作者：
Furmanik M
中科院分区：
文献类型：
--
作者：
Shanahan CM;Furmanik M
在工业化社会，心血管疾病仍然是导致死亡的主要原因。动脉平滑肌细胞（ASMC）在调节许多血管病理中起关键作用的观点越来越重要，因为人们认识到，在血管重构中调节ASMC功能的病理细胞机制还不够。在过去的十年中，内质网（ER）应激和未折叠蛋白反应（UPR）被认为是多种血管细胞类型中许多生理和病理过程的应激反应。在这里，我们总结了内质网应激信号如何调节ASMCs的表型转换、反式/去分化和凋亡，并有助于动脉粥样硬化、高血压、动脉瘤和血管钙化。
Cardiovascular disease continues to be the leading cause of death in industrialised societies. The idea that the arterial smooth muscle cell (ASMC) plays a key role in regulating many vascular pathologies has been gaining importance, as has the realisation that not enough is known about the pathological cellular mechanisms regulating ASMC function in vascular remodelling. In the past decade endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) have been recognised as a stress response underlying many physiological and pathological processes in various vascular cell types. Here we summarise what is known about how ER stress signalling regulates phenotypic switching, trans/dedifferentiation and apoptosis of ASMCs and contributes to atherosclerosis, hypertension, aneurysms and vascular calcification.