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10.1016/j.molimm.2016.11.012 http://scihub22266oqcxt.onion/10.1016/j.molimm.2016.11.012 C5366269!5366269 !27931779     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27931779 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Immunol 2017 ; 84 (ä): 57-64 Nephropedia Template TP {{tp|p=27931779 |t=2017. Complement and sepsis-induced heart dysfunction |pdf=|usr=}}{{27931779 }} gab.com Text Complement and sepsis-induced heart dysfunction JO: Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27931779 #FOAvip It is well known that cardiac dysfunction develops during sepsis in both humans and in rodents (rats, mice). These defects appear to be reversible, since after "recovery" from sepsis, cardiac dysfunction disappears and the heart returns to its function that was present before the onset of sepsis. Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis. Use of a neutralizing antibody to C5a largely attenuates cardiac dysfunction and other adverse events developing during sepsis. The molecular basis for cardiac dysfunctions is linked to generation of C5a and its interaction with C5a receptors present on surfaces of cardiomyocytes (CMs). It is established that C5a interactions with C5a receptors leads to significant reductions involving faulty contractility and relaxation in CMs. In addition, C5a interactions with C5a receptors on CMs results in reductions in Na(+)/K(+)-ATPase in CMs. This ATPase is essential for intact action potentials in CMs. The enzymatic activity and protein for this ATPase were strikingly reduced in CMs during sepsis by unknown mechanisms. In addition, C5a interactions with C5aRs also caused reductions in CM homeostatic proteins that regulate cytosolic [Ca(2+)]i in CMs: sarco/endoplasmic reticulum Ca(2+)-ATPase2 (SERCA2) and Na(+)/Ca(2+) exchanger (NCX). In the absence of C5a receptors, defects in SERCA2 and NCX in CMs after sepsis are strikingly attenuated. These observations suggest new strategies to protect the heart from dysfunction developing during sepsis. Twit Text FOAVip Complement and sepsis-induced heart dysfunction ????Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27931779 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27931779 #FOAvip English Wikipedia <ref>{{Cite pmid|27931779 }}</ref> Complement and sepsis-induced heart dysfunction #MMPMID27931779 Fattahi F ; Ward PA Mol Immunol 2017[Apr]; 84 (ä): 57-64 PMID27931779 show ga It is well known that cardiac dysfunction develops during sepsis in both humans and in rodents (rats, mice). These defects appear to be reversible, since after "recovery" from sepsis, cardiac dysfunction disappears and the heart returns to its function that was present before the onset of sepsis. Our studies, using in vivo and in vitro models, have demonstrated that C5a and its receptors (C5aR1 and C5aR2) play key roles in cardiac dysfunction developing during sepsis. Use of a neutralizing antibody to C5a largely attenuates cardiac dysfunction and other adverse events developing during sepsis. The molecular basis for cardiac dysfunctions is linked to generation of C5a and its interaction with C5a receptors present on surfaces of cardiomyocytes (CMs). It is established that C5a interactions with C5a receptors leads to significant reductions involving faulty contractility and relaxation in CMs. In addition, C5a interactions with C5a receptors on CMs results in reductions in Na(+)/K(+)-ATPase in CMs. This ATPase is essential for intact action potentials in CMs. The enzymatic activity and protein for this ATPase were strikingly reduced in CMs during sepsis by unknown mechanisms. In addition, C5a interactions with C5aRs also caused reductions in CM homeostatic proteins that regulate cytosolic [Ca(2+)]i in CMs: sarco/endoplasmic reticulum Ca(2+)-ATPase2 (SERCA2) and Na(+)/Ca(2+) exchanger (NCX). In the absence of C5a receptors, defects in SERCA2 and NCX in CMs after sepsis are strikingly attenuated. These observations suggest new strategies to protect the heart from dysfunction developing during sepsis. |Animals [MESH] |Cardiomyopathies/*etiology [MESH] |Complement C5a/*immunology [MESH] |Humans [MESH] |Myocytes, Cardiac/*immunology [MESH] |Receptor, Anaphylatoxin C5a/*immunology [MESH]Complement and sepsis-induced heart dysfunction (epmc).pdf DeepDyve Pubget Overpricing