机械敏感通道
机械生物学
罗亚
MAPK/ERK通路
细胞生物学
Rho相关蛋白激酶
信号转导
医学
机制(生物学)
趋化性
蛋白激酶A
激酶
生物信息学
神经科学
生物
内科学
离子通道
受体
哲学
认识论
作者
Vicki Vania,Lu Wang,Marco Tjakra,Tao Zhang,Juhui Qiu,Youhua Tan,Guixue Wang
标识
DOI:10.1016/j.bbadis.2019.165645
摘要
Cardiovascular diseases (CVDs) have been one of the major causes of human deaths in the world. The study of CVDs has focused on cell chemotaxis for decades. With the advances in mechanobiology, accumulating evidence has demonstrated the influence of mechanical stimuli on arterial pathophysiology and endothelial dysfunction that is a hallmark of atherosclerosis development. An increasing number of drugs have been exploited to decrease the stiffness of vascular tissue for CVDs therapy. However, the underlying mechanisms have yet to be explored. This review aims to summarize how matrix stiffness mediates atherogenesis through various important signaling pathways in endothelial cells and cellular mechanophenotype, including RhoA/Rho-associated protein kinase (ROCK), mitogen-activated protein kinase (MAPK), and Hippo pathways. We also highlight the roles of putative mechanosensitive non-coding RNAs in matrix stiffness-mediated atherogenesis. Finally, we describe the usage of tunable hydrogel and its future strategy to improve our knowledge underlying matrix stiffness-mediated CVDs mechanism.
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