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10.1089/ars.2013.5751 http://scihub22266oqcxt.onion/10.1089/ars.2013.5751 C4123469!4123469!24313895     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24313895&cmd=llinks): Failed to open stream: HTTP request failed! 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The Mechanisms and Physiological Relevance of Glycocalyx Degradation in Hepatic Ischemia/Reperfusion Injury |pdf=|usr=}}{{24313895}} gab.com Text The Mechanisms and Physiological Relevance of Glycocalyx Degradation in Hepatic Ischemia/Reperfusion Injury JO: Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24313895 #FOAvip Significance: Hepatic ischemia/reperfusion (I/R) injury is an inevitable side effect of major liver surgery that can culminate in liver failure. The bulk of I/R-induced liver injury results from an overproduction of reactive oxygen and nitrogen species (ROS/RNS), which inflict both parenchymal and microcirculatory damage. A structure that is particularly prone to oxidative attack and modification is the glycocalyx (GCX), a meshwork of proteoglycans and glycosaminoglycans (GAGs) that covers the lumenal endothelial surface and safeguards microvascular homeostasis. ROS/RNS-mediated degradation of the GCX may exacerbate I/R injury by, for example, inducing vasoconstriction, facilitating leukocyte adherence, and directly activating innate immune cells. Recent Advances: Preliminary experiments revealed that hepatic sinusoids contain a functional GCX that is damaged during murine hepatic I/R and major liver surgery in patients. There are three ROS that mediate GCX degradation: hydroxyl radicals, carbonate radical anions, and hypochlorous acid (HOCl). HOCl converts GAGs in the GCX to GAG chloramides that become site-specific targets for oxidizing and reducing species and are more efficiently fragmented than the parent molecules. In addition to ROS/RNS, the GAG-degrading enzyme heparanase acts at the endothelial surface to shed the GCX. Critical Issues: The GCX seems to be degraded during major liver surgery, but the underlying cause remains ill-defined. Future Directions: The relative contribution of the different ROS and RNS intermediates to GCX degradation in vivo, the immunogenic potential of the shed GCX fragments, and the role of heparanase in liver I/R injury all warrant further investigation. Antioxid. Redox Signal. 21, 1098?1118. Twit Text FOAVip The Mechanisms and Physiological Relevance of Glycocalyx Degradation in Hepatic Ischemia/Reperfusion Injury ????Antioxid Redox Signal http://www.kidney.de/pget.php?&tw=1&pmid=24313895 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24313895 #FOAvip English Wikipedia <ref>{{Cite pmid|24313895}}</ref> The Mechanisms and Physiological Relevance of Glycocalyx Degradation in Hepatic Ischemia/Reperfusion Injury #MMPMID24313895 van Golen RF; Reiniers MJ; Vrisekoop N; Zuurbier CJ; Olthof PB; van Rheenen J; van Gulik TM; Parsons BJ; Heger M Antioxid Redox Signal 2014[Sep]; 21 (7): 1098-118 PMID24313895show ga Significance: Hepatic ischemia/reperfusion (I/R) injury is an inevitable side effect of major liver surgery that can culminate in liver failure. The bulk of I/R-induced liver injury results from an overproduction of reactive oxygen and nitrogen species (ROS/RNS), which inflict both parenchymal and microcirculatory damage. A structure that is particularly prone to oxidative attack and modification is the glycocalyx (GCX), a meshwork of proteoglycans and glycosaminoglycans (GAGs) that covers the lumenal endothelial surface and safeguards microvascular homeostasis. ROS/RNS-mediated degradation of the GCX may exacerbate I/R injury by, for example, inducing vasoconstriction, facilitating leukocyte adherence, and directly activating innate immune cells. Recent Advances: Preliminary experiments revealed that hepatic sinusoids contain a functional GCX that is damaged during murine hepatic I/R and major liver surgery in patients. There are three ROS that mediate GCX degradation: hydroxyl radicals, carbonate radical anions, and hypochlorous acid (HOCl). HOCl converts GAGs in the GCX to GAG chloramides that become site-specific targets for oxidizing and reducing species and are more efficiently fragmented than the parent molecules. In addition to ROS/RNS, the GAG-degrading enzyme heparanase acts at the endothelial surface to shed the GCX. Critical Issues: The GCX seems to be degraded during major liver surgery, but the underlying cause remains ill-defined. Future Directions: The relative contribution of the different ROS and RNS intermediates to GCX degradation in vivo, the immunogenic potential of the shed GCX fragments, and the role of heparanase in liver I/R injury all warrant further investigation. Antioxid. Redox Signal. 21, 1098?1118. äThe Mechanisms and Physiological Relevance of Glycocalyx Degradation i(epmc).pdf DeepDyve Pubget Overpricing