Evidence map›Paper›PMID 40198689›Full record

ArticlePLoS pathogens2025

Chlamydial protease-like activity factor targets SLC7A11 for degradation to induce ferroptosis and facilitate progeny releases.

Wentao Chen, Xin Su, Yuying Pan, Han Zhou, Yidan Gao, Xuemei Wang, Lijuan Jiang, Lihong Zeng, Qingqing Xu, Xueying Yu and 7 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. RNF213-dependent lytic destruction ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Microbiology spectrum · 2026
    Article
  5. Article
  6. 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

17 authors.

Wentao ChenDermatology Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0002-4062-3865
Xin SuDepartment of Clinical Laboratory, Guangdong Provincial Second Hospital of Traditional Chinese Medicine (Guangdong Provincial Engineering Technology Research Institute of Traditional Chinese Medicine), Guangzhou, China.
Yuying PanDermatology Hospital, Southern Medical University, Guangzhou, China.
Han ZhouDermatology Hospital, Southern Medical University, Guangzhou, China.
Yidan GaoDepartment of Laboratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, China.
Xuemei WangDepartment of Laboratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, China.
Lijuan JiangDepartment of Laboratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, China.
Lihong ZengDermatology Hospital, Southern Medical University, Guangzhou, China.
Qingqing XuDermatology Hospital, Southern Medical University, Guangzhou, China.
Xueying YuDermatology Hospital, Southern Medical University, Guangzhou, China.
Xiaona YinDermatology Hospital, Southern Medical University, Guangzhou, China.
Zhanqin FengDermatology Hospital, Southern Medical University, Guangzhou, China.
Bao ZhangGuangdong Provincial Key Laboratory of Tropical Disease Research, Key Laboratory of Infectious Diseases Research in South China of Ministry of Education, School of Public Health, Southern Medical University, Guangzhou, China.
Wei ZhaoGuangdong Provincial Key Laboratory of Tropical Disease Research, Key Laboratory of Infectious Diseases Research in South China of Ministry of Education, School of Public Health, Southern Medical University, Guangzhou, China.
Yaohua XueDermatology Hospital, Southern Medical University, Guangzhou, China.
Lingli TangDepartment of Laboratory Medicine, The Second Xiangya Hospital of Central South University, Changsha, China.
Heping ZhengDermatology Hospital, Southern Medical University, Guangzhou, China.ORCID 0000-0002-9846-975X

Funding

Construction of the Pathogenic Microorganism (Toxin) Strain Resource Bank Capacity ProjectGuangdong Basic and Applied Basic Research FoundationGuangzhou Science and Technology Plan ProjectNational Natural Science Foundation of China
6 · The paper itself

Abstract

Chlamydia trachomatis, the most prevalent bacterial agent of sexually transmitted infections, poses a significant threat to reproductive health. The release of progeny through the orchestrated lysis of host cells plays a crucial role for the development of new infections, though the underlying molecular mechanisms remaining largely unexplored. In this study, we identified a novel mechanism by which Chlamydia induces host cell ferroptosis to facilitate its progeny release. This process involves the degradation of the host protein SLC7A11 by the chlamydial protease-like activity factor (CPAF), resulting in glutathione depletion and subsequent cell death characterized by lipid peroxidation. Infection with a CPAF-deficient strain fails to induce host cell ferroptosis. Notably, inhibiting ferroptosis by vitamin E reduces the Chlamydia burden in low genital tract of mice and trends toward attenuation of pathology. These findings provide new insights into the conserved survival strategies of Chlamydia and understanding of its pathogenesis.

Indexed as

Amino Acid Transport System y+Chlamydia InfectionsChlamydia trachomatisEndopeptidasesFerroptosisAnimalsFemaleHumansMiceMice, Inbred C57BLAmino Acid Transport System y+CPA factorEndopeptidasesSLC7A11 protein, human

Identifiers

PMID40198689
PMCPMC12011302

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.