Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26247933
&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
Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26247933
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Int+J+Mol+Sci
2015 ; 16
(8
): 17763-78
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Mitochondrial Mechanisms in Septic Cardiomyopathy
#MMPMID26247933
Cimolai MC
; Alvarez S
; Bode C
; Bugger H
Int J Mol Sci
2015[Aug]; 16
(8
): 17763-78
PMID26247933
show ga
Sepsis is the manifestation of the immune and inflammatory response to infection
that may ultimately result in multi organ failure. Despite the therapeutic
strategies that have been used up to now, sepsis and septic shock remain a
leading cause of death in critically ill patients. Myocardial dysfunction is a
well-described complication of severe sepsis, also referred to as septic
cardiomyopathy, which may progress to right and left ventricular pump failure.
Many substances and mechanisms seem to be involved in myocardial dysfunction in
sepsis, including toxins, cytokines, nitric oxide, complement activation,
apoptosis and energy metabolic derangements. Nevertheless, the precise underlying
molecular mechanisms as well as their significance in the pathogenesis of septic
cardiomyopathy remain incompletely understood. A well-investigated abnormality in
septic cardiomyopathy is mitochondrial dysfunction, which likely contributes to
cardiac dysfunction by causing myocardial energy depletion. A number of
mechanisms have been proposed to cause mitochondrial dysfunction in septic
cardiomyopathy, although it remains controversially discussed whether some
mechanisms impair mitochondrial function or serve to restore mitochondrial
function. The purpose of this review is to discuss mitochondrial mechanisms that
may causally contribute to mitochondrial dysfunction and/or may represent
adaptive responses to mitochondrial dysfunction in septic cardiomyopathy.