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Langer, H.T.* ; Rohm, M. ; Goncalves, M.D.* ; Sylow, L.*

AMPK as a mediator of tissue preservation: Time for a shift in dogma?

Nat. Rev. Endocrinol., DOI: 10.1038/s41574-024-00992-y (2024)
Verlagsversion Postprint DOI PMC
Open Access Green
Ground-breaking discoveries have established 5'-AMP-activated protein kinase (AMPK) as a central sensor of metabolic stress in cells and tissues. AMPK is activated through cellular starvation, exercise and drugs by either directly or indirectly affecting the intracellular AMP (or ADP) to ATP ratio. In turn, AMPK regulates multiple processes of cell metabolism, such as the maintenance of cellular ATP levels, via the regulation of fatty acid oxidation, glucose uptake, glycolysis, autophagy, mitochondrial biogenesis and degradation, and insulin sensitivity. Moreover, AMPK inhibits anabolic processes, such as lipogenesis and protein synthesis. These findings support the notion that AMPK is a crucial regulator of cell catabolism. However, studies have revealed that AMPK's role in cell homeostasis might not be as unidirectional as originally thought. This Review explores emerging evidence for AMPK as a promoter of cell survival and an enhancer of anabolic capacity in skeletal muscle and adipose tissue during catabolic crises. We discuss AMPK-activating interventions for tissue preservation during tissue wasting in cancer-associated cachexia and explore the clinical potential of AMPK activation in wasting conditions. Overall, we provide arguments that call for a shift in the current dogma of AMPK as a mere regulator of cell catabolism, concluding that AMPK has an unexpected role in tissue preservation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Activated Protein-kinase; Fatty-acid Oxidation; Stimulated Glucose-uptake; Brown Adipose-tissue; Exacerbates Insulin-resistance; Human Skeletal-muscle; Cancer Cachexia; Energy-charge; Endurance Exercise; Mammalian Target
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 1759-5029
e-ISSN 1759-5037
Zeitschrift Nature Reviews - Endocrinology
Verlag Nature Publishing Group
Verlagsort New York, NY
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes and Cancer (IDC)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-257
Förderungen German Center for Diabetes Research (DZD)
National Cancer Institute
Novo Nordisk Foundation
Independent Research Council Denmark
Danish Cancer Society
Carlsberg Foundation
European Research Council (ERC) under the European Union
Helmholtz Association - Initiative and Networking Fund
European Foundation for the Study of Diabetes (EFSD)/ Novo Nordisk Foundation Future Leaders Award
Cancer Research UK
DOI 10.1038/s41574-024-00992-y
WOS ID 001226527100001
Scopus ID 85193253699
PubMed ID 38760482
Erfassungsdatum 2024-06-14
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