Source:http://linkedlifedata.com/resource/pubmed/id/19837080
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-2-17
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pubmed:abstractText |
Vascular cells are very sensitive to their hemodynamic environment. Any change in blood pressure or blood flow can be sensed by endothelial and vascular smooth muscle cells and ultimately results in structural modifications within the vascular wall that accommodate the new conditions. In the case of hypertension, the increase in arterial stretch stimulates vessel thickening to normalize the tensile forces. This process requires modification of the extracellular matrix and of cell-matrix interactions, which mainly involves extracellular proteases. In hypertension, chronic exposure of the arterial wall to stretch leads to vascular remodeling, arterial stiffness and calcification, which finally affect target organ function. This review surveys how mechanical stretch regulates extracellular proteases, considering the signaling pathways involved and the consequences on the cardiovascular system.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1095-8584
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pubmed:author | |
pubmed:copyrightInfo |
2009 Elsevier Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
433-9
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pubmed:meshHeading |
pubmed-meshheading:19837080-Animals,
pubmed-meshheading:19837080-Extracellular Matrix,
pubmed-meshheading:19837080-Humans,
pubmed-meshheading:19837080-Hypertension,
pubmed-meshheading:19837080-NF-kappa B,
pubmed-meshheading:19837080-Peptide Hydrolases,
pubmed-meshheading:19837080-Signal Transduction
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pubmed:year |
2010
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pubmed:articleTitle |
Extracellular matrix alterations in hypertensive vascular remodeling.
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pubmed:affiliation |
Lady Davis Institute for Medical Research, McGill University, Montreal, Canada.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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