Abstract
Atherosclerosis (AS) is the leading cause of the human cardiovascular diseases (CVDs). Endothelial dysfunction promotes the monocytes infiltration and inflammation that participate fundamentally in atherogenesis. Endothelial cells (EC) have been recognized as mechanosensitive cells and have different responses to distinct mechanical stimuli. Emerging evidence shows matrix stiffness-mediated EC dysfunction plays a vital role in vascular disease, but the underlying mechanisms are not yet completely understood. This article aims to summarize the effect of matrix stiffness on the pro-atherosclerotic characteristics of EC including morphology, rigidity, biological behavior and function as well as the related mechanical signal. The review also discusses and compares the contribution of matrix stiffness-mediated phagocytosis of macrophages and EC to AS progression. These advances in our understanding of the relationship between matrix stiffness and EC dysfunction open the avenues to improve the prevention and treatment of now-ubiquitous atherosclerotic diseases.
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Acknowledgements
This study was supported by grants from the National Natural Science Key Foundation of China (Project no. 12032007), Chongqing Talents (cstc2022ycjh-bgzxm0166), the Natural Science Foundation of Chongqing in China (cstc2020jcyj-bsh0024, cstc2019jcyj-zdxmX0028).
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ZX, YC, YW, WH and WX collect the related literature materials. ZX wrote the manuscript. GW, XL and TZ provided ideas and designed the overall framework of the article.
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Xu, Z., Chen, Y., Wang, Y. et al. Matrix stiffness, endothelial dysfunction and atherosclerosis. Mol Biol Rep 50, 7027–7041 (2023). https://doi.org/10.1007/s11033-023-08502-5
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DOI: https://doi.org/10.1007/s11033-023-08502-5