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10.3233/BIR-15045 http://scihub22266oqcxt.onion/10.3233/BIR-15045 C5009627!5009627 !26600265     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26600265 &cmd=llinks): Failed to open stream: HTTP request failed! 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Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome Early forms of autodigestion |pdf=|usr=}}{{26600265 }} gab.com Text Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome Early forms of autodigestion JO: Biorheology http://www.kidney.de/pget.php?&tw=1&pmid=26600265 #FOAvip Abnormal blood rheological properties seldom occur in isolation and instead are accompanied by other complications, often designated as co-morbidities. In the metabolic syndrome with complications like hypertension, diabetes and lack of normal microvascular blood flow, the underlying molecular mechanisms that simultaneously lead to elevated blood pressure and diabetes as well as abnormal microvascular rheology and other cell dysfunctions have remained largely unknown. In this review, we propose a new hypothesis for the origin of abnormal cell functions as well as multiple co-morbidities. Utilizing experimental models for the metabolic disease with diverse co-morbidities we summarize evidence for the presence of an uncontrolled extracellular proteolytic activity that causes ectodomain receptor cleavage and loss of their associated cell function. We summarize evidence for unchecked degrading proteinase activity, e.g. due to matrix metalloproteases, in patients with hypertension, Type II diabetes and obesity, in addition to evidence for receptor cleavage in the form of receptor fragments and decreased extracellular membrane expression levels. The evidence suggest that a shift in blood rheological properties and other co-morbidities may in fact be derived from a common mechanism that is due to uncontrolled proteolytic activity, i.e. an early form of autodigestion. Identification of the particular proteases involved and the mechanisms of their activation may open the door to treatment that simultaneously targets multiple co-morbidities in the metabolic syndrome. Twit Text FOAVip Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome Early forms of autodigestion ????Biorheology http://www.kidney.de/pget.php?&tw=1&pmid=26600265 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26600265 #FOAvip English Wikipedia <ref>{{Cite pmid|26600265 }}</ref> Proteolytic receptor cleavage in the pathogenesis of blood rheology and co-morbidities in metabolic syndrome Early forms of autodigestion #MMPMID26600265 Mazor R ; Schmid-Schönbein GW Biorheology 2015[]; 52 (5-6 ): 337-52 PMID26600265 show ga Abnormal blood rheological properties seldom occur in isolation and instead are accompanied by other complications, often designated as co-morbidities. In the metabolic syndrome with complications like hypertension, diabetes and lack of normal microvascular blood flow, the underlying molecular mechanisms that simultaneously lead to elevated blood pressure and diabetes as well as abnormal microvascular rheology and other cell dysfunctions have remained largely unknown. In this review, we propose a new hypothesis for the origin of abnormal cell functions as well as multiple co-morbidities. Utilizing experimental models for the metabolic disease with diverse co-morbidities we summarize evidence for the presence of an uncontrolled extracellular proteolytic activity that causes ectodomain receptor cleavage and loss of their associated cell function. We summarize evidence for unchecked degrading proteinase activity, e.g. due to matrix metalloproteases, in patients with hypertension, Type II diabetes and obesity, in addition to evidence for receptor cleavage in the form of receptor fragments and decreased extracellular membrane expression levels. The evidence suggest that a shift in blood rheological properties and other co-morbidities may in fact be derived from a common mechanism that is due to uncontrolled proteolytic activity, i.e. an early form of autodigestion. Identification of the particular proteases involved and the mechanisms of their activation may open the door to treatment that simultaneously targets multiple co-morbidities in the metabolic syndrome. |Animals [MESH] |Hemorheology/*physiology [MESH] |Humans [MESH] |Mechanotransduction, Cellular [MESH] |Metabolic Diseases/metabolism/*pathology [MESH] |Peptide Hydrolases/*metabolism [MESH] |Receptor, Insulin/metabolism [MESH] |Receptors, Leptin/metabolism [MESH] |Vascular Endothelial Growth Factor Receptor-2/metabolism [MESH]Proteolytic receptor cleavage in the pathogenesis of blood rheology an(epmc).pdf DeepDyve Pubget Overpricing