PuSH - Publication Server of Helmholtz Zentrum München

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)
DOI PMC
Open Access Green: Postprint online available 12/2024
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.
Altmetric
Additional Metrics?
[➜Log in]
Edit extra informations Login
Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords 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
ISSN (print) / ISBN 1759-5029
e-ISSN 1759-5037
Journal Nature Reviews - Endocrinology
Publisher Nature Publishing Group
Publishing Place New York, NY
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes and Cancer (IDC)
Grants 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