Publication Date:
2014-09-23
Description:
Beyond their contribution to basic metabolism, the major cellular organelles, in particular mitochondria, can determine whether cells respond to stress in an adaptive or suicidal manner. Thus, mitochondria can continuously adapt their shape to changing bioenergetic demands as they are subjected to quality control by autophagy, or they can undergo a lethal permeabilization process that initiates apoptosis. Along similar lines, multiple proteins involved in metabolic circuitries, including oxidative phosphorylation and transport of metabolites across membranes, may participate in the regulated or catastrophic dismantling of organelles. Many factors that were initially characterized as cell death regulators are now known to physically or functionally interact with metabolic enzymes. Thus, several metabolic cues regulate the propensity of cells to activate self-destructive programs, in part by acting on nutrient sensors. This suggests the existence of "metabolic checkpoints" that dictate cell fate in response to metabolic fluctuations. Here, we discuss recent insights into the intersection between metabolism and cell death regulation that have major implications for the comprehension and manipulation of unwarranted cell loss.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219413/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219413/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, Douglas R -- Galluzzi, Lorenzo -- Kroemer, Guido -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI044828/AI/NIAID NIH HHS/ -- R01 AI047891/AI/NIAID NIH HHS/ -- R01 CA169291/CA/NCI NIH HHS/ -- R01 GM096208/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 19;345(6203):1250256. doi: 10.1126/science.1250256.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. douglas.green@stjude.org kroemer@orange.fr. ; Equipe 11 labellisee par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, F-75006 Paris, France. Universite Paris Descartes/Paris V; Sorbonne Paris Cite; F-75005 Paris, France. INSERM, U1138, F-94805 Villejuif, France. ; Equipe 11 labellisee par la Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, F-75006 Paris, France. Universite Paris Descartes/Paris V; Sorbonne Paris Cite; F-75005 Paris, France. INSERM, U1138, F-94805 Villejuif, France. Metabolomics and Cell Biology Platforms, Gustave Roussy, F-94805 Villejuif, France. Pole de Biologie, Hopital Europeen Georges Pompidou, Assistance Publique-Hopitaux de Paris, F-75015 Paris, France. douglas.green@stjude.org kroemer@orange.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25237106" target="_blank"〉PubMed〈/a〉
Keywords:
AMP-Activated Protein Kinases/metabolism
;
Acetyl Coenzyme A/metabolism
;
Animals
;
*Apoptosis
;
*Autophagy
;
*Energy Metabolism
;
Humans
;
*Metabolic Networks and Pathways
;
Mitochondria/*metabolism
;
Mitochondrial Membranes/metabolism
;
Multiprotein Complexes/metabolism
;
Permeability
;
TOR Serine-Threonine Kinases/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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