Evidence map›Paper›PMID 35211017›Full record

ReviewFrontiers in pharmacology2022

Understanding Anthracycline Cardiotoxicity From Mitochondrial Aspect.

Junqi Huang, Rundong Wu, Linyi Chen, Ziqiang Yang, Daoguang Yan, Mingchuan Li

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 3 pooled it
14.4field-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

64 citing papers in PubMed, 3 syntheses or guidelines pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Review
  7. Review
  8. The gut-heart axis in cardio-oncology.Cardiovascular research · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Variability in anthracycline dose conversions and cardiotoxicity monitoring: insights from hospital pharmacists on institutional protocols in oncology practice.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Article
  14. Article
  15. Article
  16. Review
  17. Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026
    Review
  18. Review
  19. Review
  20. Review

4 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

6 authors at 1 institution in 1 country.

Junqi HuangKey Laboratory for Regenerative Medicine, Ministry of Education, College of Life Science and Technology, Jinan University, Guangzhou, China.
Rundong WuDepartment of Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Linyi ChenDepartment of Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Ziqiang YangDepartment of Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Daoguang YanDepartment of Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Mingchuan LiDepartment of Biology, College of Life Science and Technology, Jinan University, Guangzhou, China.
Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anthracyclines, such as doxorubicin, represent one group of chemotherapy drugs with the most cardiotoxicity. Despite that anthracyclines are capable of treating assorted solid tumors and hematological malignancies, the side effect of inducing cardiac dysfunction has hampered their clinical use. Currently, the mechanism underlying anthracycline cardiotoxicity remains obscure. Increasing evidence points to mitochondria, the energy factory of cardiomyocytes, as a major target of anthracyclines. In this review, we will summarize recent findings about mitochondrial mechanism during anthracycline cardiotoxicity. In particular, we will focus on the following aspects: 1) the traditional view about anthracycline-induced reactive oxygen species (ROS), which is produced by mitochondria, but in turn causes mitochondrial injury. 2) Mitochondrial iron-overload and ferroptosis during anthracycline cardiotoxicity. 3) Autophagy, mitophagy and mitochondrial dynamics during anthracycline cardiotoxicity. 4) Anthracycline-induced disruption of cardiac metabolism.

Indexed as

anthracyclinecardiotoxicityferroptosismetabolismmitochondriamitophagyROS

Identifiers

PMID35211017
PMCPMC8861498
OpenAlexW4210943401

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.