Mechanical Reprogramming of Macrophages: A Push for Vascularization.

Mechanical Reprogramming of Macrophages: A Push for Vascularization.
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巨噬细胞的机械重编程:推动血管化。

DOI:
10.1161/atvbaha.123.319030
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发表时间:
2023
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
通讯作者:
Ramkhelawon,Bhama
Ramkhelawon,Bhama
中科院分区:
--
文献类型:
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作者:
Ramkhelawon,Bhama

文献摘要

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在过去的几十年中,组织和细胞中的环境机械压力的感知激增,通过刺激由复杂的机械感觉机制激活的不同通路来指导细胞行为。在这一期的《动脉炎、血栓形成和血管生物学》中,Xie等人1研究了机械感觉离子通道Piezo-1在调节后肢缺血后巨噬细胞血管生成反应中的作用。Piezo-1是一种膜蛋白,属于一类机械敏感性离子通道,并通过细胞膜拉伸或细胞外刚度激活,通常导致细胞溶质Ca 2+水平增加。2在这里,作者证明了腓肠肌在后肢缺血后经历动态机械过载。这与在缺血肌肉中积累的巨噬细胞升高和持续表达Piezo-1相一致。
In the past decades, there has been a surge in the appre-ciation of ambient mechanical pressures in tissues and cells that direct cellular behaviors by stimulating distinct pathways animated by sophisticated mechanosensory machinery. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Xie et al1 investigated the role of the mechanosensory ion channel Piezo-1 in regulating the angiogenic response of macrophages following hindlimb ischemia. Piezo-1 is a membrane protein that belongs to a class of mechanosensitive ion channels and is activated by cell membrane stretch or extracellular stiffness usually leading to increased cytosolic Ca2+ levels. 2 Here, the authors demonstrate that the gastrocnemius muscle undergoes dynamic mechanical overload following hindlimb ischemia. This coincided with an elevated and sustained expression of Piezo-1 by macrophages that accumulated in the ischemic muscle.