AMP-activated Protein Kinase and the Regulation of Autophagic Proteolysis

Meley, Daniel; Bauvy, Chantal; Houben-Weerts, Judith H.P.M.; Dubbelhuis, Peter F.; Helmond, Mariette T.J.; Codogno, Patrice; Meijer, Alfred J.

doi:10.1074/jbc.m605488200

Cited by 434 publications

(339 citation statements)

References 48 publications

(27 reference statements)

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“…43 Although this suppressive effect of AMPK indicated by the use of AICAR as well as metformin, another indirect AMPK activator, could be confirmed in both hepatocytes and nonhepatocytes, complementary approaches employing an AMPK inhibitor, compound C, or a dominant-negative AMPK mutant instead indicate that AMPK is required for autophagy induced by amino acid deprivation. 44 This latter finding that AMPK is a positive regulator of autophagy is supported by other studies in yeast 45 and in mammalian cells 46,47 under various conditions, including ischemia. In general, these latest observations are consistent with the dogma that AMPK can suppress TOR and TOR suppresses autophagy (Fig.…”

Section: Effect Of Energy Level and Ampk In Autophagy Induction In Hesupporting

confidence: 75%

“…44 Indeed, the AMPK-independent effects of AICAR have been observed in other cases. 48,49 Furthermore, this suppressive effect may be cell-type specific because in both murine embryonic fibroblasts and HCT116 colon cancer cells, AICAR and metformin are able to induce autophagy in a p53-dependent manner.…”

Section: Effect Of Energy Level and Ampk In Autophagy Induction In Hementioning

confidence: 99%

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Autophagy in the liver

2008

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A great part of our current understanding of mammalian macroautophagy is derived from studies of the liver. The term "autophagy" was introduced by Christian de Duve in part based on ultrastructural changes in rat liver following glucagon injection. Subsequent morphological, biochemical, and kinetics studies of autophagy in the liver defined the basic process of autophagosome formation, maturation, and degradation and the regulation of autophagy by hormones, phosphoinositide 3-kinases, and mammalian target of rapamycin. It is now clear that macroautophagy in the liver is important for the balance of energy and nutrients for basic cell functions, the removal of misfolded proteins resulting from genetic mutations or pathophysiological stimulations, and the turnover of major subcellular organelles such as mitochondria, endoplasmic reticulum, and peroxisomes under both normal and pathophysiological conditions. Disturbance of autophagy function in the liver could thus have a major impact on liver physiology and liver disease. (HEPATOLOGY 2008;47: 1773-1785.)

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Section: Effect Of Energy Level and Ampk In Autophagy Induction In Hesupporting

confidence: 75%

Section: Effect Of Energy Level and Ampk In Autophagy Induction In Hementioning

confidence: 99%

Autophagy in the liver

2008

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“…3.2 AMPK activation is associated with autophagy activation during disease progression in SOD1 G93A mice Activation of macroautophagy is an event downstream of AMPK activation and can be triggered by inhibition of mTOR (Meley et al 2006) or via ULK1 phosphorylation (Egan et al 2011, Kim et al 2011b. We next determined whether the changes in AMPK activity are also reflected by changes in autophagy.…”

Section: Ampk Activation Increases Throughout Disease Progression In mentioning

confidence: 99%

“Preconditioning” with latrepirdine, an adenosine 5′-monophosphate-activated protein kinase activator, delays amyotrophic lateral sclerosis progression in SOD1G93A mice

Coughlan

Mitchem

Hogg

et al. 2015

Neurobiology of Aging

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“…Generation of ATP via oxidative phoshorylation is inhibited during ischemia and reduced ATP levels have been shown to induce autophagy [1,10]. AMP kinase (AMPK) is involved in activating energy-generating pathways to maintain or restore ATP levels [54] and has been reported to upregulate autophagy [55][56][57]. AMPK is activated during ischemia and was recently shown to play a role in upregulaing autophagy during ischemia [10].…”

Section: Mechanisms Of Cardioprotectionmentioning

confidence: 99%

Recycle or die: The role of autophagy in cardioprotection

Gustafsson

Gottlieb

2008

Journal of Molecular and Cellular Cardiology

173

153

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Autophagy is a highly conserved cellular process responsible for the degradation of long-lived proteins and organelles. Autophagy occurs at low levels under normal conditions, but is upregulated in response to stress such as nutrient deprivation, hypoxia, mitochondrial dysfunction, and infection. Upregulation of autophagy may be beneficial to the cell by recycling of proteins to generate free amino acids and fatty acids needed to maintain energy production, by removing damaged organelles, and by preventing accumulation of protein aggragates. In contrast, there is evidence that enhanced autophagy can contribute to cell death, possibly through excessive self-digestion. In the heart, autophagy is essential role for maintaining cellular homeostasis under normal conditions and increased autophagy can be seen in conditions of starvation, ischemia/reperfusion, and heart failure. However, the functional significance of autophagy in heart disease is unclear and controversial. Here, we review the literature and discuss the evidence that autophagy can have both beneficial and detrimental roles in the myocardium depending on the level of autophagy, and discuss potential mechanisms by which autophagy provides protection in cells.

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AMP-activated Protein Kinase and the Regulation of Autophagic Proteolysis

Cited by 434 publications

References 48 publications

Autophagy in the liver

Autophagy in the liver

“Preconditioning” with latrepirdine, an adenosine 5′-monophosphate-activated protein kinase activator, delays amyotrophic lateral sclerosis progression in SOD1G93A mice

Recycle or die: The role of autophagy in cardioprotection

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