AMP-activated protein kinase confers protection against TNF-α-induced cardiac cell death

Abstract

Our data demonstrate that although DEX and MET are used as anti-inflammatory agents or insulin sensitizers, respectively, their common property to phosphorylate AMPK promotes cardiomyocyte cell survival through its regulation of Bad and the mitochondrial apoptotic mechanism.

Cells Lacking the Fumarase Tumor Suppressor Are Protected from Apoptosis through a Hypoxia-Inducible Factor-Independent, AMPK-Dependent Mechanism

“…6D): BAD was constitutively more phosphorylated and was not affected by an apoptotic stimulus in FH-deficient cells. A connection between AMPK activation and BAD phosphorylation has already been reported (9,25,45). In agreement, treatment of kidney cells with the AMPK activator AICAR resulted in increased BAD phosphorylation (Fig.…”

“…Phosphorylation of BAD impairs its antiapoptotic role at the mitochondrial level, and several kinases which signal cell survival are known to regulate BAD phosphorylation (5). Also, activated AMPK has already been reported to protect cells by increasing the level of phosphorylated BAD, likely indirectly (9,25,45). We also found inhibition of c-Jun N-terminal kinase (JNK) in FH-defective cells (Fig.…”

“…In several instances, BCL2 family proteins have been implicated in protection mediated by AMPK activation (4,9,25,26). We report here that among them, BAD is constitutively phosphorylated in FH-defective cells.…”

Compound C sensitizes Caki renal cancer cells to TRAIL-induced apoptosis through reactive oxygen species-mediated down-regulation of c-FLIPL and Mcl-1

“…It has been reported that AMPK inhibitor compound C could lead to ceramide accumulation and apoptotic cell death in MCF-7 breast carcinoma cells [6]. Moreover, several recent reports showed that AMPK activation showed anti-apoptotic effects in different cell types [20][21][22]. All these studies suggested the possibility that AMPK inhibition could play a pro-apoptotic role as well as a novel TRAIL sensitizer in cancer cells.…”

Bioenergy sensing in the brain

“…In C. elegans, activity of the LKB1/ AMPK pathway is required for conservation of lipid reserves and thereby ensures survival of the larvae through maturation. 85 Also, AMPK activity was observed to block TNFα-induced cardiomyocyte apoptosis that normally results from insults such as myocardial infarction and ischemia reperfusion, 86 suggesting a neuroprotective role of the kinase.…”