Evidence mapPaperPMID 38760482Full record

ReviewNature reviews. Endocrinology2024

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

Henning Tim Langer, Maria Rohm, Marcus DaSilva Goncalves, Lykke Sylow

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Anabolic Effects of Salbutamol Are Lost Upon Immobilization.Journal of cachexia, sarcopenia and muscle · 2025
    Trial
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. [Research Progress on Glycolytic Reprogramming and Lactylation Crosstalk in Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
  11. Review
  12. A Novel Autophagy InhibitorResearch (Washington, D.C.) · 2026
    Article
  13. Review
  14. Review
  15. Article
  16. Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025
    Review
  17. Article
  18. Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
    Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Henning Tim LangerDivision of Endocrinology, Weill Department of Medicine, Weill Cornell Medicine, New York, NY, USA. henning.langer@gmail.com.ORCID http://orcid.org/0000-0003-1838-4279
Maria RohmInstitute for Diabetes and Cancer, Helmholtz Center Munich, Neuherberg, Germany.
Marcus DaSilva GoncalvesDivision of Endocrinology, Weill Department of Medicine, Weill Cornell Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0002-0784-9248
Lykke SylowDepartment of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AMP-Activated Protein KinasesAdipose TissueAnimalsCachexiaEnergy MetabolismHumansMuscle, SkeletalNeoplasmsAMP-Activated Protein Kinases

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.