Evidence mapPaperPMID 39766321Full record

ReviewBiomolecules2024

Mitophagy in Doxorubicin-Induced Cardiotoxicity: Insights into Molecular Biology and Novel Therapeutic Strategies.

Heng Zhang, Saiyang Xie, Wei Deng

Abstract readReview
In one paragraph

Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
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  13. LncRNA HOXA11-AS Promotes Myocardial Injury in Chronic Heart Failure by Sponging miR-342-3p.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Article
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

3 authors.

Heng ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.ORCID 0009-0001-2785-2129
Saiyang XieDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.ORCID 0000-0002-5021-6315
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.ORCID 0000-0003-4883-4226

Funding

National Natural Science Foundation of China 82170245National Natural Science Foundation of China 82370284Regional Innovation and Development Joint Fund of National Natural Science Foundation of China U22A20269Research & Development plan of Hubei Province 2023BCB017
6 · The paper itself

Abstract

Doxorubicin is a chemotherapeutic drug utilized for solid tumors and hematologic malignancies, but its clinical application is hampered by life-threatening cardiotoxicity, including cardiac dilation and heart failure. Mitophagy, a cargo-specific form of autophagy, is specifically used to eliminate damaged mitochondria in autophagosomes through hydrolytic degradation following fusion with lysosomes. Recent advances have unveiled a major role for defective mitophagy in the etiology of DOX-induced cardiotoxicity. Moreover, specific interventions targeting this mechanism to preserve mitochondrial function have emerged as potential therapeutic strategies to attenuate DOX-induced cardiotoxicity. However, clinical translation is challenging because of the unclear mechanisms of action and the potential for pharmacological adverse effects. This review aims to offer fresh perspectives on the role of mitophagy in the development of DOX-induced cardiotoxicity and investigate potential therapeutic strategies that focus on this mechanism to improve clinical management.

Indexed as

CardiotoxicityDoxorubicinMitophagyAnimalsHumansDoxorubicincardiotoxicitydoxorubicinmitochondriamitophagytreatment

Identifiers

PMID39766321
PMCPMC11674137

What Socratic 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 Socratic graph.