The interplay of signaling pathway in endothelial cells-matrix stiffness dependency with targeted-therapeutic drugs
Autor: | Vicki Vania, Youhua Tan, Guixue Wang, Tao Zhang, Juhui Qiu, Lu Wang, Marco Tjakra |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
RHOA 030204 cardiovascular system & hematology Vascular Remodeling 03 medical and health sciences Mechanobiology 0302 clinical medicine Vascular Stiffness medicine Animals Humans Endothelial dysfunction Protein kinase A Molecular Biology Protein Kinase Inhibitors Randomized Controlled Trials as Topic Mitogen-Activated Protein Kinase Kinases Hippo signaling pathway Cell chemotaxis rho-Associated Kinases biology business.industry Endothelial Cells medicine.disease Atherosclerosis Elasticity Extracellular Matrix Endothelial stem cell Disease Models Animal 030104 developmental biology Treatment Outcome biology.protein Molecular Medicine Endothelium Vascular Signal transduction Hydroxymethylglutaryl-CoA Reductase Inhibitors business rhoA GTP-Binding Protein Neuroscience Signal Transduction |
Zdroj: | Biochimica et biophysica acta. Molecular basis of disease. 1866(5) |
ISSN: | 1879-260X |
Popis: | Cardiovascular diseases (CVDs) have been one of the major causes of human deaths in the world. The study of CVDs has focused on cell chemotaxis for decades. With the advances in mechanobiology, accumulating evidence has demonstrated the influence of mechanical stimuli on arterial pathophysiology and endothelial dysfunction that is a hallmark of atherosclerosis development. An increasing number of drugs have been exploited to decrease the stiffness of vascular tissue for CVDs therapy. However, the underlying mechanisms have yet to be explored. This review aims to summarize how matrix stiffness mediates atherogenesis through various important signaling pathways in endothelial cells and cellular mechanophenotype, including RhoA/Rho-associated protein kinase (ROCK), mitogen-activated protein kinase (MAPK), and Hippo pathways. We also highlight the roles of putative mechanosensitive non-coding RNAs in matrix stiffness-mediated atherogenesis. Finally, we describe the usage of tunable hydrogel and its future strategy to improve our knowledge underlying matrix stiffness-mediated CVDs mechanism. |
Databáze: | OpenAIRE |
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