Focal adhesion signaling: vascular smooth muscle cell contractility beyond calcium mechanisms.
Focal adhesion signaling: vascular smooth muscle cell contractility beyond calcium mechanisms.
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DOI：
10.1042/cs20201528
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发表时间：
2021-05-14
期刊：
影响因子：
--
通讯作者：
Krieger, Jose E
中科院分区：
文献类型：
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作者：
Ribeiro-Silva, J C;Miyakawa, A A;Krieger, Jose E
Smooth muscle cell (SMC) contractility is essential to vessel tone maintenance and blood pressure regulation. In response to vasoconstrictors, calcium-dependent mechanisms promote the activation of the regulatory myosin light chain, leading to increased cytoskeleton tension that favors cell shortening. In contrast, SMC maintain an intrinsic level of a contractile force independent of vasoconstrictor stimulation and sustained SMC contraction beyond the timescale of calcium-dependent mechanisms suggesting the involvement of additional players in the contractile response. Focal adhesions (FAs) are conceivable candidates that may influence SMC contraction. They are required for actin-based traction employed by cells to sense and respond to environmental cues in a process termed mechanotransduction. Depletion of FA proteins impairs SMC contractility, producing arteries that are prone to dissection because of a lack of mechanical stability. Here, we discuss the role of calcium-independent FA signaling mechanisms in SMC contractility. We speculate that FA signaling contributes to the genesis of a variety of SMC phenotypes and discuss the potential implications for mechanical homeostasis in normal and diseased states.
