2021
Developmental origins of mechanical homeostasis in the aorta
Murtada S, Kawamura Y, Li G, Schwartz MA, Tellides G, Humphrey JD. Developmental origins of mechanical homeostasis in the aorta. Developmental Dynamics 2021, 250: 629-639. PMID: 33341996, PMCID: PMC8089041, DOI: 10.1002/dvdy.283.Peer-Reviewed Original ResearchConceptsPostnatal days P2Intramural cellsSmooth muscle contractilityLate prenatal periodBlood pressureDays P2Muscle contractilityAortic structureMurine aortaPrenatal periodEndothelial cellsAortaPathological conditionsAortic developmentDeposition of matrixDevelopmental originsMatrix depositionHomeostasisHomeostatic stateCellsIntramural stressPressure-induced mechanical stressFlow-induced shear stressMechanical loadingContractility
2009
Mechanotransduction in vascular physiology and atherogenesis
Hahn C, Schwartz MA. Mechanotransduction in vascular physiology and atherogenesis. Nature Reviews Molecular Cell Biology 2009, 10: 53-62. PMID: 19197332, PMCID: PMC2719300, DOI: 10.1038/nrm2596.Peer-Reviewed Original ResearchConceptsImportant regulatory factorEndothelial extracellular matrixBiochemical signalsGene expressionBlood pressureRegulatory factorsCellular responsesRegions of arteriesFluid shear stressBlood flowExtracellular matrixPhysiological responsesProgression of atherosclerosisSystemic risk factorsNormal physiological responseMechanical forcesChronic inflammationPhysiologyVascular physiologyRisk factorsHigh cholesterolVascular endotheliumAtherosclerosisBlood vesselsCells
2006
A mechanosensory complex that mediates the endothelial cell response to fluid shear stress
Tzima E, Irani‐Tehrani M, Kiosses W, Dejana E, Schultz D, Engelhardt B, Cao G, DeLisser H, Schwartz M. A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. The FASEB Journal 2006, 20: a1378-a1378. DOI: 10.1096/fasebj.20.5.a1378-c.Peer-Reviewed Original ResearchPECAM-1-null miceDownstream inflammatory genesPECAM-1VE-cadherinDevelopment of atherosclerosisICAM-1 expressionNF-kB activationInitiation of atherosclerosisBlood pressureVascular remodelingHigh-affinity stateInflammatory genesNF-κBCell responsesEndothelial cell responsesNull miceMechanosensory complexIntegrin activationAffinity stateAtherosclerosisVEGFR2Heterologous cellsPathway upstreamActivationSrc family kinases