Evidence map›Paper›PMID 26160707›Full record

ReviewTrends in endocrinology and metabolism: TEM2015

AMPK: energy sensor and survival mechanism in the ischemic heart.

Dake Qi, Lawrence H Young

Abstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed
–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

155 citing papers in PubMed.

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  11. GLP-1 activates KNature communications · 2026
    Article
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95 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

2 authors.

Dake QiThe Sections of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA.
Lawrence H YoungThe Sections of Cardiovascular Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA; Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA; Department of Cellular and Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. Box 208017, New Haven, CT 06520-8017, USA. Electronic address: Lawrence.young@yale.edu.

Funding

DDT and CD74 receptor activation prevent cardiac injuryR01HL128069 · NHLBI · YALE UNIVERSITY · PI YOUNG, LAWRENCE H · 2015 to 2018
$1.7M
NHLBI NIH HHS HL128069NHLBI NIH HHS R01 HL128069
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is a critical regulator of cellular metabolism and plays an important role in diabetes, cancer, and vascular disease. In the heart, AMPK activation is an essential component of the adaptive response to cardiomyocyte stress that occurs during myocardial ischemia. During ischemia-reperfusion, AMPK activation modulates glucose and fatty acid metabolism, mitochondrial function, endoplasmic reticulum (ER) stress, autophagy, and apoptosis. Pharmacological activation of AMPK prevents myocardial necrosis and contractile dysfunction during ischemia-reperfusion and potentially represents a cardioprotective strategy for the treatment of myocardial infarction. This review discusses novel mechanisms of AMPK activation in the ischemic heart, the role of endogenous AMPK activation during ischemia, and the potential therapeutic applications for AMPK-directed therapy.

Indexed as

AMP-Activated Protein KinasesAnimalsHumansMyocardial IschemiaMyocardial Reperfusion InjuryAMP-Activated Protein Kinases

Identifiers

PMID26160707
PMCPMC4697457

What OpenQuestion holds

Textmetadata
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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.