Evidence mapPaperPMID 40969268Full record

ReviewFrontiers in oncology2025

The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment.

Feilong Chen, Lei Lyu, Chengyuan Xing, Yu Chen, Shaofan Hu, Meng Wang, Zhengdong Ai

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

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

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Journal of thoracic disease · 2026
    Article
  15. Article
  16. Review
  17. Chronic Cholestatic Liver Disease Induced by Larval Ascariasis: Novel Insights Into Immune-Mediated Pathogenesis and Hepatic Fibrosis in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  18. Review
  19. Article
  20. 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

7 authors.

Feilong ChenSports Medicine Key Laboratory of Sichuan Province, Expert Centre of Sichuan Province, Institute of Sports Medicine and Health, Chengdu Sport University, Chengdu, China.
Lei LyuSports Medicine Key Laboratory of Sichuan Province, Expert Centre of Sichuan Province, Institute of Sports Medicine and Health, Chengdu Sport University, Chengdu, China.
Chengyuan XingSports Medicine Key Laboratory of Sichuan Province, Expert Centre of Sichuan Province, Institute of Sports Medicine and Health, Chengdu Sport University, Chengdu, China.
Yu ChenSports Medicine Key Laboratory of Sichuan Province, Expert Centre of Sichuan Province, Institute of Sports Medicine and Health, Chengdu Sport University, Chengdu, China.
Shaofan HuJinfeng Laboratory, Chongqing, China.
Meng WangDepartment of Pathophysiology, College of High Altitude Military Medicine, Third Military Medical University (Army Medical University), Chongqing, China.
Zhengdong AiInstitute for Cancer Medicine, School of Basic Medical Sciences, Southwest Medical University, Luzhou, Sichuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis, which is characterized by pathological extracellular matrix (ECM) accumulation impairing organ function, is governed primarily by dysregulated transforming growth factor-β (TGF-β)/Smad signalling. TGF-β1 triggers canonical (Smad2/3-dependent) and noncanonical pathways upon receptor binding, driving profibrotic processes such as fibroblast activation, epithelial-mesenchymal transition (EMT), excessive ECM production (e.g., collagen), and the suppression of matrix degradation. This pathway is central to organ-specific fibrogenesis: In liver fibrosis, it activates hepatic stellate cells (HSCs); in renal fibrosis, it promotes tubular injury and ECM deposition; in pulmonary fibrosis, it induces EMT/fibroblast transition in radiation/bleomycin models; in cardiac fibrosis, it mediates fibroblast activation in diabetic cardiomyopathy/atrial fibrillation via NPRC/TGIF1/USP mechanisms; and in skin fibrosis (e.g., scleroderma), it stimulates collagen overproduction, which is suppressed by osthole or mesenchymal stem cells. The TGF-β/Smad axis thus represents a pivotal therapeutic target. Future research should clarify tissue-specific regulatory networks and develop combinatorial antifibrotic strategies.

Indexed as

ECMEMTfibrosismiRNATGF-β/Smad signalling pathway

Identifiers

PMID40969268
PMCPMC12440922

What Socratic holds

Textmetadata
LicenceCC BY
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.