Evidence map›Paper›PMID 42310666›Full record

ReviewJournal of ovarian research2026

Mechanisms of mitochondrial dysfunction in premature ovarian insufficiency.

Chenyu Jia, Huihui Li, Ruotong Ju, Puhua Zhang, Li Peng, Tingting Xue, Xinyu Zhu, Shu Wang, Jiali Luo, Ruixiang Zhu and 2 more

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

12 authors.

Chenyu JiaDepartment of Reproductive Medicine Center, Children's Hospital of Shanxi, The Affiliated Children's Hospital of Shanxi Medical University, Shanxi Maternal and Child Health Hospital, Taiyuan, 030001, China.
Huihui LiDepartment of Reproductive Medicine Center, Children's Hospital of Shanxi, The Affiliated Children's Hospital of Shanxi Medical University, Shanxi Maternal and Child Health Hospital, Taiyuan, 030001, China.
Ruotong JuDepartment of Reproductive Medicine Center, Children's Hospital of Shanxi, The Affiliated Children's Hospital of Shanxi Medical University, Shanxi Maternal and Child Health Hospital, Taiyuan, 030001, China.
Puhua ZhangDepartment of Reproductive Medicine Center, Children's Hospital of Shanxi, The Affiliated Children's Hospital of Shanxi Medical University, Shanxi Maternal and Child Health Hospital, Taiyuan, 030001, China.
Li PengDepartment of Shanxi Hospital of Integrated Traditional and Western Medicine, Shanxi University of Traditional Chinese Medicine, Taiyuan, 030001, China.
Tingting XueDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China.
Xinyu ZhuDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China.
Shu WangDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China.
Jiali LuoDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China.
Ruixiang ZhuDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China.
Xuan JingDepartment of Clinical Laboratory, Shanxi Provincial People's Hospital, Shanxi Medical University, Taiyuan, 030001, China. jx05070103@163.com.
Xiangrong CuiDepartment of Reproductive Medicine Center, Children's Hospital of Shanxi, The Affiliated Children's Hospital of Shanxi Medical University, Shanxi Maternal and Child Health Hospital, Taiyuan, 030001, China. cuixiangrong094030@163.com.

Funding

Basic Research Project of Shanxi Province 202403021221275Research Project Supported by Shanxi Scholarship Council of China 2025-225Scientific Research Project of Shanxi Provincial Health Commission 2025QM021the Young Top-notch Talent in the Healthcare System under the Sanjin Talent Program of Shanxi Province SJYC2025500
6 · The paper itself

Abstract

Premature ovarian insufficiency (POI) is a clinical syndrome characterized by the decline of ovarian function in women under the age of 40, and its core pathological feature is the irreversible depletion of the ovarian reserve. Mitochondria serve as the central hub for energy metabolism and signal integration in ovarian cells, and their dysfunction drives POI progression through multiple cell death pathways and signaling cascades. This review systematically examines the multidimensional mechanisms by which mitochondrial damage leads to follicle depletion and proposes, for the first time, an integrated regulatory model termed "mitochondrial damage - follicle fate decision." The review further identifies contradictory evidence, model limitations, and gaps in clinical translation within current research. Regarding therapeutic strategies, we evaluate the current status, safety risks, and ethical barriers of mitochondrial nutrients, stem cell therapy, gene editing, and mitochondrial replacement therapy. Finally, we propose a future research framework centered on mitochondrial dynamics and quality control, emphasizing the need for multi-omics integration and personalized interventions.

Indexed as

MitochondriaPrimary Ovarian InsufficiencyAnimalsFemaleHumansSignal TransductionFollicular atresiaGranulosa cell deathMitochondrial dysfunctionPremature ovarian insufficiency

Identifiers

PMID42310666
PMCPMC13520522

What Socratic 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 Socratic graph.