Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

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.

10.1038/s41467-025-66978-0 http://scihub22266oqcxt.onion/10.1038/s41467-025-66978-0 41339353!?!41339353 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41339353&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       Nat+Commun 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41339353|t=2025. Platelet-mediated activation of perivascular mast cells triggers progression of sepsis to septic shock in mice |pdf=|usr=}}{{41339353}} gab.com Text Platelet-mediated activation of perivascular mast cells triggers progression of sepsis to septic shock in mice JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=41339353 #FOAvip The critical events that trigger sepsis progression into life-threatening septic shock remain unclear. In agreement with reports that link a drop in platelet count to a complicated clinical course in sepsis patients, here we report that, during sepsis, mouse platelets become activated, deposit systemically on vascular walls, and stimulate perivascular mast cells (MC) by releasing platelet activating factor (PAF). In mouse models and patient samples, MC activation correlates with the development of shock in sepsis and is mechanistically linked to shock by inducing systemic hypotension, vascular leakage and microvascular perfusion abnormalities. Preventing platelet or MC activation, or inhibiting the activity of the major MC granule constituent chymase, averts progression from sepsis to shock and reduces mortality of septic mice. Thus, our work establishes that, during sepsis progression, platelet microvascular adhesion leads to MC-mediated vascular changes to culminate in septic shock and septic shock-associated mortality. Twit Text FOAVip Platelet-mediated activation of perivascular mast cells triggers progression of sepsis to septic shock in mice ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=41339353 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41339353 #FOAvip English Wikipedia <ref>{{Cite pmid|41339353}}</ref> Platelet-mediated activation of perivascular mast cells triggers progression of sepsis to septic shock in mice #MMPMID41339353 Choi HW; Noh JH; Iskarpatyoti J; Zhu X; Bao C; Abraham M; Hoffmann U; Privratsky JR; Lee RH; Bergmeier W; Tsalik EL; Fiorino C; Yao J; Abraham SN; Karhausen J Nat Commun 2025[Dec]; ? (?): ? PMID41339353show ga The critical events that trigger sepsis progression into life-threatening septic shock remain unclear. In agreement with reports that link a drop in platelet count to a complicated clinical course in sepsis patients, here we report that, during sepsis, mouse platelets become activated, deposit systemically on vascular walls, and stimulate perivascular mast cells (MC) by releasing platelet activating factor (PAF). In mouse models and patient samples, MC activation correlates with the development of shock in sepsis and is mechanistically linked to shock by inducing systemic hypotension, vascular leakage and microvascular perfusion abnormalities. Preventing platelet or MC activation, or inhibiting the activity of the major MC granule constituent chymase, averts progression from sepsis to shock and reduces mortality of septic mice. Thus, our work establishes that, during sepsis progression, platelet microvascular adhesion leads to MC-mediated vascular changes to culminate in septic shock and septic shock-associated mortality. ?Platelet-mediated activation of perivascular mast cells triggers progr(epmc).pdf DeepDyve Pubget Overpricing