Evidence map›Paper›PMID 38744846›Full record

ReviewSignal transduction and targeted therapy2024

Mitochondrial dysfunction: mechanisms and advances in therapy.

Yao Zong, Hao Li, Peng Liao, Long Chen, Yao Pan, Yongqiang Zheng, Changqing Zhang, Delin Liu, Minghao Zheng, Junjie Gao

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 693 papers.

0numbers the graph read from it
0cells of the map it votes in
693citing 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

693 citing papers in PubMed.

  1. Trial
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  8. Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026
    Review
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  11. Article
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  13. Review
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  15. Article
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  20. Review

633 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

10 authors.

Yao Zong *Centre for Orthopaedic Research, Medical School, The University of Western Australia, Nedlands, WA, 6009, Australia.
Hao Li *Department of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Peng LiaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.ORCID 0000-0002-4583-5285
Long ChenState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, CAS Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, 200031, China.
Yao PanDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Yongqiang ZhengSixth People's Hospital Fujian, No. 16, Luoshan Section, Jinguang Road, Luoshan Street, Jinjiang City, Quanzhou, Fujian, China.
Changqing ZhangDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.
Delin LiuDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China. delin.liu@research.uwa.edu.au.
Minghao ZhengCentre for Orthopaedic Research, Medical School, The University of Western Australia, Nedlands, WA, 6009, Australia. minghao.zheng@uwa.edu.au.ORCID 0000-0003-1185-4768
Junjie GaoDepartment of Orthopaedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China. colingjj@163.com.ORCID 0000-0003-4820-8524

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82002339
6 · The paper itself

Abstract

Mitochondria, with their intricate networks of functions and information processing, are pivotal in both health regulation and disease progression. Particularly, mitochondrial dysfunctions are identified in many common pathologies, including cardiovascular diseases, neurodegeneration, metabolic syndrome, and cancer. However, the multifaceted nature and elusive phenotypic threshold of mitochondrial dysfunction complicate our understanding of their contributions to diseases. Nonetheless, these complexities do not prevent mitochondria from being among the most important therapeutic targets. In recent years, strategies targeting mitochondrial dysfunction have continuously emerged and transitioned to clinical trials. Advanced intervention such as using healthy mitochondria to replenish or replace damaged mitochondria, has shown promise in preclinical trials of various diseases. Mitochondrial components, including mtDNA, mitochondria-located microRNA, and associated proteins can be potential therapeutic agents to augment mitochondrial function in immunometabolic diseases and tissue injuries. Here, we review current knowledge of mitochondrial pathophysiology in concrete examples of common diseases. We also summarize current strategies to treat mitochondrial dysfunction from the perspective of dietary supplements and targeted therapies, as well as the clinical translational situation of related pharmacology agents. Finally, this review discusses the innovations and potential applications of mitochondrial transplantation as an advanced and promising treatment.

Indexed as

MitochondriaAnimalsCardiovascular DiseasesDNA, MitochondrialHumansMicroRNAsMitochondrial DiseasesNeoplasmsNeurodegenerative DiseasesDNA, MitochondrialMicroRNAs

Identifiers

PMID38744846
PMCPMC11094169

What OpenQuestion holds

Textmetadata
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.