Evidence map›Paper›PMID 39366483›Full record

ReviewJournal of advanced research2025

The role of JNK signaling pathway in organ fibrosis.

Min Hao, Yandan Lu, Zhouhui Yao, Pingping Wang, Ziyan Chen, Licheng Zhou, Qiao Yang, Xianan Sang, Kuilong Wang, Gang Cao

Abstract readReview
In one paragraph

Review in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

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

  1. Pooled it
  2. Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Endothelin-1 drives COX-2 and prostaglandin EJournal of dental sciences · 2026
    Article
  8. Article
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

10 authors.

Min HaoSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China; Songyang Research Institute of Zhejiang Chinese Medical University, Songyang, 323400, China.
Yandan LuSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Zhouhui YaoSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Pingping WangSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Ziyan ChenSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Licheng ZhouSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Qiao YangSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Xianan SangSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China; Songyang Research Institute of Zhejiang Chinese Medical University, Songyang, 323400, China. Electronic address: sangxianan@zcmu.edu.cn.
Kuilong WangSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China. Electronic address: kuilongwang@zcmu.edu.cn.
Gang CaoSchool of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China. Electronic address: caog1984@zcmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibrosis is a tissue damage repair response caused by multiple pathogenic factors which could occur in almost every apparatus and leading to the tissue structure damage, physiological abnormality, and even organ failure until death. Up to now, there is still no specific drugs or strategies can effectively block or changeover tissue fibrosis. JNKs, a subset of mitogen-activated protein kinases (MAPK), have been reported that participates in various biological processes, such as genetic expression, DNA damage, and cell activation/proliferation/death pathways. Increasing studies indicated that abnormal regulation of JNK signal pathway has strongly associated with tissue fibrosis. AIM OF REVIEW: This review designed to sum up the molecular mechanism progresses in the role of JNK signal pathway in organ fibrosis, hoping to provide a novel therapy strategy to tackle tissue fibrosis. KEY SCIENTIFIC CONCEPTS OF REVIEW: Recent evidence shows that JNK signaling pathway could modulates inflammation, immunoreaction, oxidative stress and Multiple cell biological functions in organ fibrosis. Therefore, targeting the JNK pathway may be a useful strategy in cure fibrosis.

Indexed as

FibrosisJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemAnimalsHumansOxidative StressSignal TransductionJNK Mitogen-Activated Protein KinasesJNK signaling pathwayMolecular mechanismOrgan fibrosisSmall-molecule inhibitorTreatment strategy

Identifiers

PMID39366483
PMCPMC12302471

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.