Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Multiple facets of NF-kappaB in the heart: to be or not to NF-kappaB Gordon JW; Shaw JA; Kirshenbaum LACirc Res 2011[Apr]; 108 (9): 1122-32The progression from cardiac injury to symptomatic heart failure has been intensely studied over the last decade, and is largely attributable to a loss of functional cardiac myocytes through necrosis, intrinsic and extrinsic apoptosis pathways and autophagy. Therefore, the molecular regulation of these cellular programs has been rigorously investigated in the hopes of identifying a potential cell target that could promote cell survival and/or inhibit cell death to avert, or at least prolong, the degeneration toward symptomatic heart failure. The nuclear factor (NF)-kappaB super family of transcription factors has been implicated in the regulation of immune cell maturation, cell survival, and inflammation in many cell types, including cardiac myocytes. Recent studies have shown that NF-kappaB is cardioprotective during acute hypoxia and reperfusion injury. However, prolonged activation of NF-kappaB appears to be detrimental and promotes heart failure by eliciting signals that trigger chronic inflammation through enhanced elaboration of cytokines including tumor necrosis factor alpha, interleukin-1, and interleukin-6, leading to endoplasmic reticulum stress responses and cell death. The underlying mechanisms that account for the multifaceted and differential outcomes of NF-kappaB on cardiac cell fate are presently unknown. Herein, we posit a novel paradigm in which the timing, duration of activation, and cellular context may explain mechanistically the differential outcomes of NF-kappaB signaling in the heart that may be essential for future development of novel therapeutic interventions designed to target NF-kappaB responses and heart failure following myocardial injury.|*Heart Failure/metabolism/pathology/physiopathology[MESH]|Animals[MESH]|Apoptosis/*physiology[MESH]|Autophagy/physiology[MESH]|Cytokines/physiology[MESH]|Humans[MESH]|Myocytes, Cardiac/*pathology/physiology[MESH]|NF-kappa B/*physiology[MESH]|Necrosis[MESH] |
