Evidence map›Paper›PMID 39781451›Full record

ArticleInternational journal of biological sciences2025

USP25 stabilizes STAT6 to promote IL-4-induced macrophage M2 polarization and fibrosis.

Yahan Xu, Jing Liu, Jingzeng Wang, Jiayao Wang, Peixiang Lan, Tao Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Yahan XuDepartment of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Jing LiuInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Jingzeng WangInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Jiayao WangDepartment of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Peixiang LanInstitute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Organ Transplantation, Ministry of Education; NHC Key Laboratory of Organ Transplantation; Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, China.
Tao WangDepartment of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As a leading cause of morbidity and mortality, fibrosis is the common pathway of various chronic inflammatory diseases in organs and causes death in a large number of patients. It can destroy the structure and function of organs and ultimately lead to organ failure, which is a major cause of disability and death in many diseases. However, the regulatory mechanism of organ fibrosis is not well clear and the lack of effective drugs and treatments, which seriously endangers human health and safety. In this study, we found that ubiquitin specific peptidases 25 (USP25) deficiency could protect mice from bleomycin (BLM)-induced pulmonary fibrosis and bile duct ligation (BDL)-induced liver fibrosis. Mechanistically, USP25 deficiency reduced the infiltration of M2 macrophages in the lungs and livers. USP25 inhibits signal transducer and activator of transcription 6 / peroxisome proliferator-activated receptor gamma (STAT6/PPAR-γ) signaling by reducing the K48 specific ubiquitination of STAT6, thereby promoting IL-4-induced M2 macrophages. Overall, our findings support that USP25 promotes the development of fibrosis by facilitating macrophage M2 polarization.

Indexed as

Interleukin-4MacrophagesSTAT6 Transcription FactorUbiquitin ThiolesteraseAnimalsBleomycinFibrosisHumansLiver CirrhosisMaleMiceMice, Inbred C57BLPulmonary FibrosisSignal TransductionUbiquitinationBleomycinInterleukin-4Stat6 protein, mouseSTAT6 Transcription FactorUbiquitin Thiolesterase

Identifiers

PMID39781451
PMCPMC11705635

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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.