Evidence map›Paper›PMID 37731615›Full record

ArticleiScience2023

Mitochondrial transplantation ameliorates doxorubicin-induced cardiac dysfunction via activating glutamine metabolism.

Xiaolei Sun, Hang Chen, Rifeng Gao, Ya Huang, Yanan Qu, Heng Yang, Xiang Wei, Shiyu Hu, Jian Zhang, Peng Wang and 4 more

Abstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
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  11. Causes of and Solutions to Mitochondrial Disorders: A Literature Review.International journal of molecular sciences · 2025
    Review
  12. Review
  13. Review
  14. 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

14 authors.

Xiaolei SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Hang ChenDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Rifeng GaoShanghai Fifth People's Hospital, Fudan University, Shanghai 200240, P.R. China.
Ya HuangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Yanan QuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Heng YangThe Second Affiliated Hospital of Nanchang University, Nanchang 330000, P.R. China.
Xiang WeiShanghai Fifth People's Hospital, Fudan University, Shanghai 200240, P.R. China.
Shiyu HuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Jian ZhangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Peng WangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Yunzeng ZouDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Kai HuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
Aijun SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Doxorubicin is a wildly used effective anticancer agent. However, doxorubicin use is also related to cardiotoxic side effect in some patients. Mitochondrial damage has been shown to be one of the pathogeneses of doxorubicin-induced myocardial injury. In this study, we demonstrated that mitochondrial transplantation could inhibit doxorubicin-induced cardiotoxicity by directly supplying functional mitochondria. Mitochondrial transplantation improved contractile function and respiratory capacity, reduced cellular apoptosis and oxidative stress in cardiomyocytes. Mitochondria isolated from various sources, including mouse hearts, mouse and human arterial blood, and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), all exerted similar cardioprotective effects. Mechanically, mitochondrial transplantation activates glutamine metabolism in doxorubicin-treated mice heart and blocking glutamine metabolism attenuated the cardioprotective effects of mitochondrial transplantation. Overall, our study demonstrates that mitochondria isolated from arterial blood could be used for mitochondrial transplantation, which might serve as a feasible promising therapeutic option for patients with doxorubicin-induced cardiotoxicity.

Indexed as

BiochemistryCell biologyCellular physiologyMetabolomicsMolecular physiology

Identifiers

PMID37731615
PMCPMC10507231

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.