Evidence map›Paper›PMID 27108839›Full record

ReviewNature reviews. Nephrology2016

TGF-β: the master regulator of fibrosis.

Xiao-Ming Meng, David J Nikolic-Paterson, Hui Yao Lan

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05637216 (A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients), which is not on this map. Cited by 2,054 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2,054citing papers in PubMed, 1 pooled it
102.5field-weighted citation impact, top 1% of its field
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.

NCT05637216 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients

TypeinterventionalSponsorShaw Cancer CenterRan2023 to 2027Enrolled43ConditionsRadiation Induced FibrosisArmsLosartan 25 milligram capsule, Placebo
3 · Its place in the literature

Who cites it

2,054 citing papers in PubMed, 1 synthesis or guideline pooled it, 3,352 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  11. Article
  12. Galectin-3 Mediates TGF-β-Controlled Migration in Müller Glial Cells.International journal of molecular sciences · 2026
    Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

1,994 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 2 countries.

Xiao-Ming MengSchool of Pharmacy and Institute for Kidney Diseases, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.
David J Nikolic-PatersonDepartment of Nephrology and Monash University Department of Medicine, 246 Clayton Road, Monash Medical Centre, Clayton, Victoria 3168, Australia.
Hui Yao LanDepartment of Medicine &Therapeutics and Li Ka Shing Institute of Health Sciences, and Shenzhen Research Institute, The Chinese University of Hong Kong, Prince of Wales Hospital, 30-32 Ngan Shing Street, Shatin, The New Territories, Hong Kong, China.
Anhui Medical University · CNMonash University · AUPrince of Wales Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) is the primary factor that drives fibrosis in most, if not all, forms of chronic kidney disease (CKD). Inhibition of the TGF-β isoform, TGF-β1, or its downstream signalling pathways substantially limits renal fibrosis in a wide range of disease models whereas overexpression of TGF-β1 induces renal fibrosis. TGF-β1 can induce renal fibrosis via activation of both canonical (Smad-based) and non-canonical (non-Smad-based) signalling pathways, which result in activation of myofibroblasts, excessive production of extracellular matrix (ECM) and inhibition of ECM degradation. The role of Smad proteins in the regulation of fibrosis is complex, with competing profibrotic and antifibrotic actions (including in the regulation of mesenchymal transitioning), and with complex interplay between TGF-β/Smads and other signalling pathways. Studies over the past 5 years have identified additional mechanisms that regulate the action of TGF-β1/Smad signalling in fibrosis, including short and long noncoding RNA molecules and epigenetic modifications of DNA and histone proteins. Although direct targeting of TGF-β1 is unlikely to yield a viable antifibrotic therapy due to the involvement of TGF-β1 in other processes, greater understanding of the various pathways by which TGF-β1 controls fibrosis has identified alternative targets for the development of novel therapeutics to halt this most damaging process in CKD.

Indexed as

AnimalsFibrosisHistonesHumansKidneyMicroRNAsRenal Insufficiency, ChronicSignal TransductionSmad ProteinsTransforming Growth Factor betaHistonesMicroRNAsSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID27108839
OpenAlexW2342679639

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.