Evidence map›Paper›PMID 41761224›Full record

ReviewJournal of ovarian research2026

Dual regulation of PINK1/PARKIN-mediated mitochondrial autophagy in ovarian cancer progression and drug resistance: mechanisms and therapeutic potentials.

Jing Xu, Fangyuan Liu, Qiaochu Chen, Yue Li, Jaifei Liu, Fengjuan Han

Abstract readReview
In one paragraph

Review in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jing XuDepartment of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Fangyuan LiuDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Qiaochu ChenDepartment of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Yue LiDepartment of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Jaifei LiuDepartment of Obstetrics and Gynecology, Heilongjiang University of Chinese Medicine, Harbin, 150040, China.
Fengjuan HanDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, 150040, China. hanfengjuan2004@163.com.

Funding

National Natural Science Foundation of China 82274566
6 · The paper itself

Abstract

Ovarian cancer (OC) is a common primary female malignancy globally. It is characterized by a high rate of confirmed diagnosis at an advanced stage (around 70%), abdominal and distant metastases at initial diagnosis, and relatively lower average 5-year survival rate worldwide (< 30%). This undoubtedly greatly increases the difficulty and complexity of the treatment. The therapeutic effect of OC is primarily compromised by the mechanism of chemotherapy resistance, which is complex and has not been fully elucidated. Beyond producing negative impact on the effectiveness of existing treatment strategies, the resistance of cancer cells to chemotherapeutic agents may also prompt the medical community to constantly explore new treatment approaches. Therefore, in order to develop more effective treatment plans, it highlights the importance and necessity of achieving a thorough understanding of the pathogenesis of OC and the mechanism of chemotherapy resistance. Currently, mitophagy, an intracellular self-degradation process, has been documented to be pivotal in the development of OC and in chemotherapy resistance. It functions to maintain the stability of the intracellular environment through the autophagy mechanism, regulate cellular energy metabolism, and participate in immune responses, supporting its potential of inhibiting tumor growth theoretically. In particular, the PINK1/PARKIN pathway demonstrates a unique bidirectional regulatory effect in tumor growth regulation and chemotherapy resistance reversal. Its dynamic regulatory mechanism in platinum-based resistance of OC has revealed potential therapeutic targets. Accordingly, with emphasis on the bidirectional regulatory role of the PINK1/PARKIN signaling pathway-mediated mitophagy in inhibiting the growth of OC and reversing chemotherapy resistance, this study aimed to integrate the latest research results, and provide innovative treatment strategies and ideas for OC treatment and chemotherapy efficacy optimization.

Indexed as

Drug Resistance, NeoplasmMitochondriaOvarian NeoplasmsProtein KinasesUbiquitin-Protein LigasesAnimalsAutophagyDisease ProgressionFemaleHumansMitophagyPTEN-Induced Putative KinaseSignal Transductionparkin proteinProtein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein LigasesChemotherapy resistanceMechanismsMitophagyOvarian cancerPINK1/PARKIN

Identifiers

PMID41761224
PMCPMC13214074

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Registered trials

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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.