Document Detail

An emerging role of degrading proteinases in hypertension and the metabolic syndrome: autodigestion and receptor cleavage.
MedLine Citation:
PMID:  22081429     Owner:  NLM     Status:  MEDLINE    
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.
Geert W Schmid-Schönbein
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current hypertension reports     Volume:  14     ISSN:  1534-3111     ISO Abbreviation:  Curr. Hypertens. Rep.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-06     Completed Date:  2012-05-01     Revised Date:  2014-09-17    
Medline Journal Info:
Nlm Unique ID:  100888982     Medline TA:  Curr Hypertens Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  88-96     Citation Subset:  IM    
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MeSH Terms
Extracellular Matrix Proteins / metabolism*
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
Reg. No./Substance:
0/Extracellular Matrix Proteins; 0/Receptors, Cell Surface; EC 3.4.24.-/Matrix Metalloproteinases

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