Evidence map›Paper›PMID 39160244›Full record

ArticleActa pharmacologica Sinica2025

Otilonium bromide ameliorates pulmonary fibrosis in mice through activating phosphatase PPM1A.

Tong Zhao, Zhi-Ruo Zhou, Hui-Qi Wan, Tian Feng, Xu-Hui Hu, Xiao-Qian Li, Shi-Mei Zhao, Hong-Lin Li, Ji-Wei Hou, Wei Li and 3 more

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 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. Roles of the E3 Ubiquitin Ligase TRIM47 in Inflammation, Organ Injury, and Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  2. Article
  3. Article
  4. Blocking TRIM47-mediated HNF4Acta pharmaceutica Sinica. B · 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

13 authors.

Tong Zhao *Jiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Zhi-Ruo Zhou *Jiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Hui-Qi WanJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Tian FengJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Xu-Hui HuSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Xiao-Qian LiJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Shi-Mei ZhaoJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Hong-Lin LiJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Ji-Wei HouJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Wei LiSchool of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Da-Yun LuJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. dayunlu@njucm.edu.cn.
Min-Yi QianJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. qianmy@njucm.edu.cn.
Xu ShenJiangsu Key Laboratory of Drug Target and Drug for Degenerative Diseases, School of Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. xshen@njucm.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is a chronic, progressive and irreversible interstitial lung disease characterized by unremitting pulmonary myofibroblasts activation, extracellular matrix (ECM) deposition and inflammatory recruitment. PF has no curable medication yet. In this study we investigated the molecular pathogenesis and potential therapeutic targets of PF and discovered drug lead compounds for PF therapy. A murine PF model was established in mice by intratracheal instillation of bleomycin (BLM, 5 mg/kg). We showed that the protein level of pulmonary protein phosphatase magnesium-dependent 1A (PPM1A, also known as PP2Cα) was significantly downregulated in PF patients and BLM-induced PF mice. We demonstrated that TRIM47 promoted ubiquitination and decreased PPM1A protein in PF progression. By screening the lab in-house compound library, we discovered otilonium bromide (OB, clinically used for treating irritable bowel syndrome) as a PPM1A enzymatic activator with an EC

Indexed as

BleomycinMice, Inbred C57BLProtein Phosphatase 2CPulmonary FibrosisQuaternary Ammonium CompoundsAnimalsDisease Models, AnimalHumansLungMiceSmad3 ProteinTripartite Motif ProteinsUbiquitinationUbiquitin-Protein LigasesBleomycinoctyloniumPPM1A protein, humanPpm1a protein, mouseProtein Phosphatase 2CQuaternary Ammonium CompoundsSmad3 ProteinTripartite Motif ProteinsUbiquitin-Protein LigasesNLRP3otilonium bromidePPM1Apulmonary fibrosisSMAD3

Identifiers

PMID39160244
PMCPMC11695943

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.