Evidence map›Paper›PMID 28445146›Full record

ReviewOncotarget2017

Autophagy and mitophagy in the context of doxorubicin-induced cardiotoxicity.

Navid Koleini, Elissavet Kardami

Registry-linked trialOpen access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07070765 (Sodium-glucose Transporter Type 2 Inhibition in Anthracycline-related Cardiotoxicity - SPRINT), which is not on this map. Cited by 150 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 3 pooled it
16.9field-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.

NCT07070765 narecruitingnot on this mapstarted 2025, after this paper: background citation

Sodium-glucose Transporter Type 2 Inhibition in Anthracycline-related Cardiotoxicity - SPRINT

TypeinterventionalSponsorUniversity of AberdeenRan2025 to 2028Enrolled70ConditionsBreast CancerArmsSodium-glucose transport-2 (SGLT-2) inhibitors, Standard medical treatment
3 · Its place in the literature

Who cites it

150 citing papers in PubMed, 3 syntheses or guidelines pooled it, 302 citations in OpenAlex.

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90 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.

Navid KoleiniInstitute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Manitoba, Canada.
Elissavet KardamiInstitute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Manitoba, Canada.
St. Boniface Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin (Dox) is a cytotoxic drug widely incorporated in various chemotherapy protocols. Severe side effects such as cardiotoxicity, however, limit Dox application. Mechanisms by which Dox promotes cardiac damage and cardiomyocyte cell death have been investigated extensively, but a definitive picture has yet to emerge. Autophagy, regarded generally as a protective mechanism that maintains cell viability by recycling unwanted and damaged cellular constituents, is nevertheless subject to dysregulation having detrimental effects for the cell. Autophagic cell death has been described, and has been proposed to contribute to Dox-cardiotoxicity. Additionally, mitophagy, autophagic removal of damaged mitochondria, is affected by Dox in a manner contributing to toxicity. Here we will review Dox-induced cardiotoxicity and cell death in the broad context of the autophagy and mitophagy processes.

Indexed as

AnimalsAntibiotics, AntineoplasticAutophagyBiomarkersCardiotoxicityDoxorubicinHeart DiseasesHumansMitochondria, HeartMitophagyMyocytes, CardiacSignal TransductionAntibiotics, AntineoplasticBiomarkersDoxorubicinanthracyclinesheart failureimpaired autophagy and mitophagylysosomal dysfunctiononcocardiology

Identifiers

PMID28445146
PMCPMC5542301
OpenAlexW2604294853

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.