{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Walther BK"],"funding":["NIBIB NIH HHS","Directorate for Engineering","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","Texas A and M University","National Institute of Biomedical Imaging and Bioengineering","National Science Foundation"],"pagination":["1738-1751"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9761985"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(9)"],"pubmed_abstract":["Endothelial mechanobiology is a key consideration in the progression of vascular dysfunction, including atherosclerosis. However mechanistic connections between the clinically associated physical stimuli, vessel stiffness and shear stress, and how they interact to modulate plaque progression remain incompletely characterized. Vessel-chip systems are excellent candidates for modeling vascular mechanobiology as they may be engineered from the ground up, guided by the mechanical parameters present in human arteries and veins, to recapitulate key features of the vasculature. Here, we report extensive validation of a vessel-chip model of endothelial yes-associated protein (YAP) mechanobiology, a protein sensitive to both matrix stiffness and shearing forces and, importantly, implicated in ather"],"journal":["Lab on a chip"],"pubmed_title":["Mechanotransduction-on-chip: vessel-chip model of endothelial YAP mechanobiology reveals matrix stiffness impedes shear response."],"pmcid":["PMC9761985"],"funding_grant_id":["1944322","1R01HL133254","R21EB025945","R01 HL133254","1R01HL148338","R21 EB025945"],"pubmed_authors":["Kilic ES","Guiseppi-Elie A","Gold KA","Gaharwar AK","Jain A","Sama V","Walther BK","Cooke JP","Rajeeva Pandian NK","Gu J"],"additional_accession":[]},"is_claimable":false,"name":"Mechanotransduction-on-chip: vessel-chip model of endothelial YAP mechanobiology reveals matrix stiffness impedes shear response.","description":"Endothelial mechanobiology is a key consideration in the progression of vascular dysfunction, including atherosclerosis. However mechanistic connections between the clinically associated physical stimuli, vessel stiffness and shear stress, and how they interact to modulate plaque progression remain incompletely characterized. Vessel-chip systems are excellent candidates for modeling vascular mechanobiology as they may be engineered from the ground up, guided by the mechanical parameters present in human arteries and veins, to recapitulate key features of the vasculature. Here, we report extensive validation of a vessel-chip model of endothelial yes-associated protein (YAP) mechanobiology, a protein sensitive to both matrix stiffness and shearing forces and, importantly, implicated in ather","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-26T09:50:30.465Z","creation":"2025-04-06T13:08:09.757Z"},"accession":"S-EPMC9761985","cross_references":{"pubmed":["33949409"],"doi":["10.1039/d0lc01283a"]}}