Evidence map›Paper›PMID 19275766›Full record

ReviewClinical science (London, England : 1979)2009

AMP-activated protein kinase pathway: a potential therapeutic target in cardiometabolic disease.

Aaron K F Wong, Jacqueline Howie, John R Petrie, Chim C Lang

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 1% of its field
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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Journal of experimental pharmacology · 2024
    Article
  10. Review
  11. Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023
    Review
  12. Time-of-day defines NADNature communications · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

14 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Aaron K F WongDivision of Medicine and Therapeutics, University of Dundee and Medical School, Ninewells Hospital, Dundee DD1 9SY, Scotland, UK.
Jacqueline Howie
John R Petrie
Chim C Lang
Ninewells Hospital · GB

Funding

British Heart Foundation PG/06/143/21897
6 · The paper itself

Abstract

AMPK (AMP-activated protein kinase) is a heterotrimetric enzyme that is expressed in many tissues, including the heart and vasculature, and plays a central role in the regulation of energy homoeostasis. It is activated in response to stresses that lead to an increase in the cellular AMP/ATP ratio caused either by inhibition of ATP production (i.e. anoxia or ischaemia) or by accelerating ATP consumption (i.e. muscle contraction or fasting). In the heart, AMPK activity increases during ischaemia and functions to sustain ATP, cardiac function and myocardial viability. There is increasing evidence that AMPK is implicated in the pathophysiology of cardiovascular and metabolic diseases. A principle mode of AMPK activation is phosphorylation by upstream kinases [e.g. LKB1 and CaMK (Ca(2+)/calmodulin-dependent protein kinase], which leads to direct effects on tissues and phosphorylation of various downstream kinases [e.g. eEF2 (eukaryotic elongation factor 2) kinase and p70 S6 kinase]. These upstream and downstream kinases of AMPK have fundamental roles in glucose metabolism, fatty acid oxidation, protein synthesis and tumour suppression; consequently, they have been implicated in cardiac ischaemia, arrhythmias and hypertrophy. Recent mechanistic studies have shown that AMPK has an important role in the mechanism of action of MF (metformin), TDZs (thiazolinediones) and statins. Increased understanding of the beneficial effects of AMPK activation provides the rationale for targeting AMPK in the development of new therapeutic strategies for cardiometabolic disease.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesCardiovascular DiseasesEnzyme ActivationEnzyme ActivatorsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMetabolic SyndromeMetforminRibonucleotidesSignal TransductionThiazolidinedionesAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesEnzyme ActivatorsHydroxymethylglutaryl-CoA Reductase InhibitorsMetforminRibonucleotidesThiazolidinediones

Identifiers

PMID19275766
PMCPMC2762688
OpenAlexW2067136301

What OpenQuestion holds

Texttitle and abstract
LicenceCC BY-NC
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 OpenQuestion graph.