Evidence map›Paper›PMID 32034646›Full record

ReviewCardiovascular drugs and therapy2020

The Role of AMPK Activation for Cardioprotection in Doxorubicin-Induced Cardiotoxicity.

Kerstin N Timm, Damian J Tyler

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular drugs and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 2 pooled it
14.8field-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

90 citing papers in PubMed, 2 syntheses or guidelines pooled it, 175 citations in OpenAlex.

  1. Pooled it
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  14. Article
  15. Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025
    Review
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  18. Article
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30 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 at 1 institution in 1 country.

Kerstin N TimmDepartment of Physiology Anatomy and Genetics, University of Oxford, Oxford, UK. kerstin.timm@dpag.ox.ac.uk.ORCID 0000-0001-9136-7518
Damian J TylerDepartment of Physiology Anatomy and Genetics, University of Oxford, Oxford, UK.
University of Oxford · GB

Funding

British Heart Foundation FS/14/17/30634British Heart Foundation FS/16/7/31843British Heart Foundation FS/19/18/34252British Heart Foundation RG/11/9/28921Medical Research Council G0601490
6 · The paper itself

Abstract

Doxorubicin is a commonly used chemotherapeutic agent for the treatment of a range of cancers, but despite its success in improving cancer survival rates, doxorubicin is cardiotoxic and can lead to congestive heart failure. Therapeutic options for this patient group are limited to standard heart failure medications with the only drug specific for doxorubicin cardiotoxicity to reach FDA approval being dexrazoxane, an iron-chelating agent targeting oxidative stress. However, dexrazoxane has failed to live up to its expectations from preclinical studies while also bringing up concerns about its safety. Despite decades of research, the molecular mechanisms of doxorubicin cardiotoxicity are still poorly understood and oxidative stress is no longer considered to be the sole evil. Mitochondrial impairment, increased apoptosis, dysregulated autophagy and increased fibrosis have also been shown to be crucial players in doxorubicin cardiotoxicity. These cellular processes are all linked by one highly conserved intracellular kinase: adenosine monophosphate-activated protein kinase (AMPK). AMPK regulates mitochondrial biogenesis via PGC1α signalling, increases oxidative mitochondrial metabolism, decreases apoptosis through inhibition of mTOR signalling, increases autophagy through ULK1 and decreases fibrosis through inhibition of TGFβ signalling. AMPK therefore sits at the control point of many mechanisms shown to be involved in doxorubicin cardiotoxicity and cardiac AMPK signalling itself has been shown to be impaired by doxorubicin. In this review, we introduce different agents known to activate AMPK (metformin, statins, resveratrol, thiazolidinediones, AICAR, specific AMPK activators) as well as exercise and dietary restriction, and we discuss the existing evidence for their potential role in cardioprotection from doxorubicin cardiotoxicity.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsAntibiotics, AntineoplasticCaloric RestrictionCardiotoxicityDoxorubicinEnzyme ActivationEnzyme ActivatorsExerciseHeart DiseasesHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMetforminMitochondria, HeartMyocytes, CardiacAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesAntibiotics, AntineoplasticDoxorubicinEnzyme ActivatorsHydroxymethylglutaryl-CoA Reductase InhibitorsMetforminResveratrolRibonucleotidesThiazolidinedionesAICARAMPKCardiotoxicityDoxorubicinMetformin

Identifiers

PMID32034646
PMCPMC7125062
OpenAlexW3004664745

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.