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10.1681/ASN.2017010069 http://scihub22266oqcxt.onion/10.1681/ASN.2017010069 C5491297!5491297 !28465380     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28465380 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28465380 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Am+Soc+Nephrol 2017 ; 28 (7 ): 1973-1982 Nephropedia Template TP {{tp|p=28465380 |t=2017. The Angiopoietin-Tie2 Signaling Axis in Systemic Inflammation |pdf=|usr=}}{{28465380 }} gab.com Text The Angiopoietin-Tie2 Signaling Axis in Systemic Inflammation JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28465380 #FOAvip Systemic inflammation is a hallmark of commonly encountered diseases ranging from bacterial sepsis to sterile syndromes such as major trauma. Derangements in the host vasculature contribute to the cardinal manifestations of sepsis in profound ways. Recent studies of control pathways regulating the vascular endothelium have illuminated how this single cell layer toggles between quiescence and activation to affect the development of shock and multiorgan dysfunction. This article focuses on one such control pathway, the Tie2 receptor and its ligands the angiopoietins, to describe a growing body of genetic, biochemical, mechanistic, and human studies that implicate Tie2 as a critical switch. In health, activated Tie2 maintains the endothelium in a quiescent state characterized by dynamic barrier function and antiadhesion against circulating leukocytes. In sepsis and related diseases, expression of the angiopoietins becomes markedly imbalanced and Tie2 signaling is greatly attenuated. These rapid molecular changes potentiate pathophysiologic responses throughout the body, resulting in injurious vascular leakage and organ inflammation. The Tie2 axis, therefore, may be a promising avenue for future translational studies. Twit Text FOAVip The Angiopoietin-Tie2 Signaling Axis in Systemic Inflammation ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=28465380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28465380 #FOAvip English Wikipedia <ref>{{Cite pmid|28465380 }}</ref> The Angiopoietin-Tie2 Signaling Axis in Systemic Inflammation #MMPMID28465380 Parikh SM J Am Soc Nephrol 2017[Jul]; 28 (7 ): 1973-1982 PMID28465380 show ga Systemic inflammation is a hallmark of commonly encountered diseases ranging from bacterial sepsis to sterile syndromes such as major trauma. Derangements in the host vasculature contribute to the cardinal manifestations of sepsis in profound ways. Recent studies of control pathways regulating the vascular endothelium have illuminated how this single cell layer toggles between quiescence and activation to affect the development of shock and multiorgan dysfunction. This article focuses on one such control pathway, the Tie2 receptor and its ligands the angiopoietins, to describe a growing body of genetic, biochemical, mechanistic, and human studies that implicate Tie2 as a critical switch. In health, activated Tie2 maintains the endothelium in a quiescent state characterized by dynamic barrier function and antiadhesion against circulating leukocytes. In sepsis and related diseases, expression of the angiopoietins becomes markedly imbalanced and Tie2 signaling is greatly attenuated. These rapid molecular changes potentiate pathophysiologic responses throughout the body, resulting in injurious vascular leakage and organ inflammation. The Tie2 axis, therefore, may be a promising avenue for future translational studies. |*Signal Transduction [MESH] |Angiopoietins/*physiology [MESH] |Animals [MESH] |Humans [MESH] |Inflammation/*etiology [MESH]The Angiopoietin-Tie2 Signaling Axis in Systemic Inflammation (epmc).pdf DeepDyve Pubget Overpricing