Evidence map›Paper›PMID 41252074›Full record

ArticleScience China. Life sciences2026

Plat safeguards maternally aged oocytes against programmed cell death through activating the Erk1/2 pathway.

Xingsi He, Hanwen Zhang, Ya Wang, Huanyu Yan, Qiuzhen Chen, Min Su, Qiaozhen Shi, Xiao Zeng, Wei Sheng, Yangmin Wang and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

15 authors.

Xingsi He *State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Hanwen Zhang *State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Ya Wang *State Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Huanyu YanState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Qiuzhen ChenState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Min SuState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Qiaozhen ShiDepartment of Laboratory Medicine, Taikang Xianlin Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210046, China.
Xiao ZengState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Wei ShengState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Yangmin WangState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Chikun WangState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Shuyue HouState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Zhibin HuState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China.
Yuanlin HeState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China. yuanlinhe@njmu.edu.cn.
Xi WangState Key Laboratory of Reproductive Medicine and Offspring Health, Center for Clinical Reproductive Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 211166, China. xiwang@njmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The decline in oocyte quality and developmental potential with female reproductive aging is well recognized, yet the underlying mechanisms remain insufficiently investigated. In this study, an integrative analysis of transcriptomes and morphologies of individual oocytes from young and aged mice identifies morphologically defective aged oocytes with distinct transcriptomic features. Further analysis demonstrates that both apoptotic and ferroptotic pathways are activated in the defective aged oocytes, and simultaneously blocking both pathways reverses the defective morphology to the largest extent. The Plat gene, which encodes tissue-type plasminogen activator (tPA), is down-regulated with oocyte aging, and Plat knockdown increases oocyte susceptibility to both apoptosis and ferroptosis. Mechanistically, tPA functions as an upstream signaling molecule for Erk1/2 activation by interacting with particular phosphorylation kinases such as Alk. Consequently, Plat loss downregulates Erk1/2 pathway activity in oocytes, leading to degeneration through PCD. Supplementing exogenous tPA in vitro oocyte maturation cultures reduces the defect rate of aged oocytes, thereby improving oocyte quality and developmental potential. Collectively, Plat plays a pivotal role in protecting aged mouse oocytes from PCD, and tPA supplementation may serve as a potential clinical strategy to enhance oocyte quality in females of advanced maternal age.

Indexed as

ApoptosisMAP Kinase Signaling SystemOocytesTissue Plasminogen ActivatorAnimalsCellular SenescenceFemaleMiceTissue Plasminogen ActivatorapoptosisERK1/2 pathwayferroptosisoocyte agingprogrammed cell deathtPA/PLAT

Identifiers

What OpenQuestion holds

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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.