Biomechanics-mediated endocytosis in atherosclerosis

Biomechanical forces, including vascular shear stress, cyclic stretching, and extracellular matrix stiffness, which influence mechanosensitive channels in the plasma membrane, determine cell function in atherosclerosis. Being highly associated with the formation of atherosclerotic plaques, endocytos...

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Published inFrontiers in cardiovascular medicine Vol. 11; p. 1337679
Main Authors Wang, Jinxuan, Xu, Jianxiong, Liu, Tianhu, Yu, Chaoping, Xu, Fengcheng, Wang, Guixue, Li, Shun, Dai, Xiaozhen
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 04.04.2024
Subjects
atherosclerosis
biomechanics
Cardiovascular Medicine
endocytosis
lipid transportation
vascular cells
atherosclerosis
vascular cells
endocytosis
biomechanics
lipid transportation
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Summary:Biomechanical forces, including vascular shear stress, cyclic stretching, and extracellular matrix stiffness, which influence mechanosensitive channels in the plasma membrane, determine cell function in atherosclerosis. Being highly associated with the formation of atherosclerotic plaques, endocytosis is the key point in molecule and macromolecule trafficking, which plays an important role in lipid transportation. The process of endocytosis relies on the mobility and tension of the plasma membrane, which is sensitive to biomechanical forces. Several studies have advanced the signal transduction between endocytosis and biomechanics to elaborate the developmental role of atherosclerosis. Meanwhile, increased plaque growth also results in changes in the structure, composition and morphology of the coronary artery that contribute to the alteration of arterial biomechanics. These cross-links of biomechanics and endocytosis in atherosclerotic plaques play an important role in cell function, such as cell phenotype switching, foam cell formation, and lipoprotein transportation. We propose that biomechanical force activates the endocytosis of vascular cells and plays an important role in the development of atherosclerosis.
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Yong Chen, Nanchang University, China
Reviewed by: Yoshinari Uehara, Fukuoka University, Japan
Edited by: Angeliki Chroni, National Centre of Scientific Research Demokritos, Greece
Abbreviations LDL, low density lipoprotein; VLDL, very low density lipoprotein; LDLR, low density lipoprotein receptor; ECs, endothelial cells; LSS, Low shear stress; OSS, oscillatory shear stress; APs, adaptor proteins; oxLDL, oxidized low-density lipoprotein; Cav1, caveolin-1; VSMCs, vascular smooth muscle cells; NO, nitric oxide; TRP, transient receptor potential; ROS, reactive oxygen species.
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2024.1337679