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by the rickettsiae(passive) to be causedInjury to endothelium and vascular smooth muscle cells infected by R rickettsii seems
These hemodynamic and neurohumoral alterationscan causevascular endothelial cell damage and hypertrophic change in the vascular smooth muscle cells
directly ... the rickettsiae , possibly through the activity of a rickettsial phospholipase or rickettsial protease or through free - radical peroxidation of host cell membranes(passive) to be caused ... byInjury to endothelium and vascular smooth muscle cells infected by R rickettsii seems
a large block of DNA , known as the 9p21.3 cardiovascular risk haplotypecausesabnormalities in vascular smooth muscular cells
in this geneleadto death of smooth muscle cells in the aorta
Nitric oxidecausesapoptosis in pulmonary vascular smooth muscle cells
both human hypertension and experimental models of hypertension ... increased intravascular pressurecausesconstriction of vascular smooth muscle cells ( VSMCs ) in resistant arteries
the tyrosine kinase pathway causing the release of calcium ions from intracellular storageresultingin smooth muscle contraction of cerebral arteries
endothelial TLR9 activityresultingin pulmonary vascular smooth muscle cell activation
Oxidative stressleadsto cholesterol accumulation in vascular smooth muscle cells
NOX4 downregulationleadsto senescence of human vascular smooth muscle cells
the MVs circulating in the plasma of elderly subjectscontributetowards the calcification of vascular smooth muscle cells
the different pathwayscan leadto endothelium - dependent hyperpolarization of the vascular smooth muscle cells
Blache D. Oxidative stressleadsto cholesterol accumulation in vascular smooth muscle cells
PI3 Kresultingin apoptosis of vascular smooth muscle cells
the vasoactive peptide endothelincontributesto vasoconstriction in vascular smooth muscle cells
nitric oxidecausingstimulation of guanylate cyclase in the vascular smooth muscle cells
Adenosinecausesconstriction of the vascular smooth muscle cells of the afferent arteriole
Multiple repressor pathwayscontributeto phenotypic switching of vascular smooth muscle cells
by endothelium - derived and exogenous NO as well as those due to endothelium - dependent hyperpolarization(passive) caused byin smooth muscle cells of the porcine coronary artery , Kaempferol enhanced relaxations
the diseased vessels ... macrophagesledto the predominance of vascular smooth muscle cells in blood vessel walls
ROCK has an effect on translocation of ERK1 to the cellular nucleusleadingto proliferation of smooth muscle cells in the pulmonary artery
pathwaycausesvascular smooth muscle cells to proliferate
Reactive oxygen species ( ROSoriginating predominantlyfrom vascular smooth muscle cells ( VSMCs
Extensive proliferation of a subset of differentiated , yet plasticcontributesmedial vascular smooth muscle cells
in plaque rupture and thrombosismay resultin plaque rupture and thrombosis
occlusion of the vesselscausesocclusion of the vessels
to heart diseasecan leadto heart disease
to atherosclerosis and restenosiscontributesto atherosclerosis and restenosis
an increase in blood flowcausesan increase in blood flow
restenosis(passive) is caused byrestenosis
to a numbercontributesto a number
to reduced arterial elasticity , hypotension , and an impaired arterial response to angiotensin II in vivoledto reduced arterial elasticity , hypotension , and an impaired arterial response to angiotensin II in vivo
to hypoxic pulmonary hypertensioncontributesto hypoxic pulmonary hypertension
to myocardialcan leadto myocardial
to vascularremodelingleadingto vascularremodeling
to hypoxic pulmonary hypertensioncontributesto hypoxic pulmonary hypertension
ATP availability(passive) caused byATP availability
symptoms(passive) caused bysymptoms
Vasodilation(passive) caused byVasodilation
Vasodilation(passive) caused byVasodilation
reduced vessel responsiveness to local rheological stimuli and reduced luminal diameter with consequent increased microvascular resistance during times of increased myocardial oxygen demandcausingreduced vessel responsiveness to local rheological stimuli and reduced luminal diameter with consequent increased microvascular resistance during times of increased myocardial oxygen demand
to vascular tone and homeostasiscontributeto vascular tone and homeostasis
to reduction of the lumen arealeadsto reduction of the lumen area
vascular remodeling(passive) caused byvascular remodeling
to narrowing and obliteration of the vessel lumen resulting in increased vascular toneleadingto narrowing and obliteration of the vessel lumen resulting in increased vascular tone
to in - stent restenosis ( ISRleadingto in - stent restenosis ( ISR
in alterations of their matrix producing propertiesresultingin alterations of their matrix producing properties
to neointima formationleadsto neointima formation
This neointima(passive) is composedThis neointima
to occlusive vascular diseases by virtue of their ability to switch to a noncontractile , migratory , and proliferating phenotypecontribute significantlyto occlusive vascular diseases by virtue of their ability to switch to a noncontractile , migratory , and proliferating phenotype