机械应力调控血管平滑肌细胞的凋亡.

BACKGROUND: With the development of biomechanics, its research into cardiovascular diseases has become more and more extensive. By studying the mechanical properties of blood vessels, the pathogenesis of cardiovascular diseases such as atherosclerosis and restenosis can be effectively revealed and new ideas and methods can be developed for the treatment of cardiovascular diseases. OBJECTIVE: To review the research status of apoptosis of vascular smooth muscle cells induced by mechanical stress and search for potential target molecules and signaling pathways for clinical treatment, thereby improving the clinical treatment effect on cardiovascular diseases such as atherosclerosis and restenosis. METHODS: We searched the literature in CNKI, PubMed and ScienceDirect databases from January 1992 to May 2023. The search terms were “vascular smooth muscle cell, mechanical stress, shear stress, stretch stress, apoptosis” in Chinese and English. Finally, 63 articles were included for review and analysis. RESULTS AND CONCLUSION: Physiological and pathological apoptosis of vascular smooth muscle cells is an adaptive remodeling in response to the changes in vascular mechanics. Vascular smooth muscle cells in different parts have different mechanical stimuli and their pathogenesis is also different. Low shear stress, physiological shear stress and high shear stress directly interact with surface molecules, receptors and proteins of vascular smooth muscle cells to regulate apoptosis-related signaling molecules and inhibit cell proliferation, thus regulating the apoptosis of vascular smooth muscle cells. In this part, the research on promoting proliferation is not summarized. Low stretch stress, physiological stretch stress and high stretch stress can all cause apoptosis of vascular smooth muscle cells, but it is still controversial. There are many mechanoreceptors (such as integrins and receptor tyrosine kinases) on the surface of vascular smooth muscle cells, which can transform mechanical signals into intracellular chemical signals (such as the Hippo pathway), activate the apoptosis signals of vascular smooth muscle cells and regulate the apoptosis of vascular smooth muscle cells. In short, different mechanical stimuli start a variety of signal pathways and regulate the apoptosis of vascular smooth muscle cells through various signal molecules. For example, shear stress affects Fas/FasL and Akt pathways mainly by stimulating prostaglandin secretion and transforming growth factors. Strech stress mainly regulates the YAP pathway and Notch pathway through Yes-related proteins. At different times or intensities, these molecules may play opposite two-way roles. For example, when mouse vascular smooth muscle cells are stretched at 10% physiological tension for 1 hour, cell proliferation increases. However, the proliferation of human vascular smooth muscle cells can decrease after 12 hours of stretching. Clinically, the key molecules of mechanical transduction can be disturbed by searching for key molecules that interfere with mechanical transduction at their critical time points of action. [ABSTRACT FROM AUTHOR]