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A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1155/2016/2183026 http://scihub22266oqcxt.onion/10.1155/2016/2183026 C4835650!4835650 !27127546     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27127546 &cmd=llinks): Failed to open stream: HTTP request failed! 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ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury |pdf=|usr=}}{{27127546 }} gab.com Text ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=27127546 #FOAvip Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated. Twit Text FOAVip ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=27127546 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27127546 #FOAvip English Wikipedia <ref>{{Cite pmid|27127546 }}</ref> ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury #MMPMID27127546 Minutoli L ; Puzzolo D ; Rinaldi M ; Irrera N ; Marini H ; Arcoraci V ; Bitto A ; Crea G ; Pisani A ; Squadrito F ; Trichilo V ; Bruschetta D ; Micali A ; Altavilla D Oxid Med Cell Longev 2016[]; 2016 (ä): 2183026 PMID27127546 show ga Ischemia and reperfusion (I/R) causes a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to the ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, and inflammatory responses to cell death. In normal conditions, ROS mediate important beneficial responses. When their production is prolonged or elevated, harmful events are observed with peculiar cellular changes. In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. The mechanisms underlying the activation of NLRP3 are several and not completely elucidated. It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Aim of the present review is to describe the current knowledge on the role of NLRP3 in some organs (brain, heart, kidney, and testis) after I/R injury, with particular regard to the role played by ROS in its activation. Furthermore, as no specific therapy for the prevention or treatment of the high mortality and morbidity associated with I/R is available, the state of the art of the development of novel therapeutic approaches is illustrated. |Animals [MESH] |Brain/metabolism/pathology [MESH] |Inflammasomes/*metabolism [MESH] |Kidney/metabolism [MESH] |Male [MESH] |Myocardium/*metabolism [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism [MESH] |Reactive Oxygen Species/*metabolism [MESH] |Reperfusion Injury/metabolism/*pathology [MESH]ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, an(epmc).pdf DeepDyve Pubget Overpricing