| An emerging role of degrading proteinases in hypertension and the metabolic syndrome: autodigestion and receptor cleavage. | |
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MedLine Citation:
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PMID: 22081429 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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One of the major challenges for hypertension research is to identify the mechanisms that cause the comorbidities encountered in many hypertensive patients, as seen in the metabolic syndrome. An emerging body of evidence suggests that human and experimental hypertensives may exhibit uncontrolled activity of proteinases, including the family of matrix metalloproteinases, recognized for their ability to restructure the extracellular matrix proteins and to play a role in hypertrophy. We propose a new hypothesis that provides a molecular framework for the comorbidities of hypertension, diabetes, capillary rarefaction, immune suppression, and other cell and organ dysfunctions due to early and uncontrolled extracellular receptor cleavage by active proteinases. The proteinase and signaling activity in hypertensives requires further detailed analysis of the proteinase expression, the mechanisms causing proenzyme activation, and identification of the proteinase substrate. This work may open the opportunity for reassessment of old interventions and development of new interventions to manage hypertension and its comorbidities. |
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Authors:
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Geert W Schmid-Schönbein |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Current hypertension reports Volume: 14 ISSN: 1534-3111 ISO Abbreviation: Curr. Hypertens. Rep. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-01-06 Completed Date: 2012-05-01 Revised Date: 2013-05-23 |
Medline Journal Info:
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Nlm Unique ID: 100888982 Medline TA: Curr Hypertens Rep Country: United States |
Other Details:
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Languages: eng Pagination: 88-96 Citation Subset: IM |
Affiliation:
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Department of Bioengineering, Institute of Engineering in Medicine, University of California San Diego, La Jolla, CA 92093-0412, USA. gwss@ucsd.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Comorbidity Extracellular Matrix Proteins / metabolism* Humans Hypertension / complications, enzymology*, physiopathology Hypertrophy / enzymology Immune Tolerance / physiology Matrix Metalloproteinases / metabolism* Metabolic Syndrome X / complications, enzymology*, physiopathology Microcirculation / physiology Models, Biological Receptors, Cell Surface / metabolism* Renin-Angiotensin System / physiology Signal Transduction / physiology* Vasoconstriction / physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL 10881/HL/NHLBI NIH HHS; R01 HL010881-44/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Extracellular Matrix Proteins; 0/Receptors, Cell Surface; EC 3.4.24.-/Matrix Metalloproteinases |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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