Evidence map›Paper›PMID 39934355›Full record

ReviewNature reviews. Nephrology2025

Advances and challenges in kidney fibrosis therapeutics.

Lilia Abbad, Emmanuel Esteve, Christos Chatziantoniou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. The efficacy ofRenal failure · 2026
    Article
  4. Article
  5. Article
  6. T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

3 authors.

Lilia AbbadINSERM UMR S 1155, Common and Rare Kidney Diseases, Tenon Hospital, Faculty of Medicine, Sorbonne University, Paris, France.ORCID 0000-0001-6548-6935
Emmanuel EsteveINSERM UMR S 1155, Common and Rare Kidney Diseases, Tenon Hospital, Faculty of Medicine, Sorbonne University, Paris, France.ORCID 0000-0003-3656-8557
Christos ChatziantoniouINSERM UMR S 1155, Common and Rare Kidney Diseases, Tenon Hospital, Faculty of Medicine, Sorbonne University, Paris, France. christos.chatziantoniou@sorbonne-universite.fr.ORCID 0000-0003-4440-099X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a major global health burden that affects more than 10% of the adult population. Current treatments, including dialysis and transplantation, are costly and not curative. Kidney fibrosis, defined as an abnormal accumulation of extracellular matrix in the kidney parenchyma, is a common outcome in CKD, regardless of disease aetiology, and is a major cause of loss of kidney function and kidney failure. For this reason, research efforts have focused on identifying mediators of kidney fibrosis to inform the development of effective anti-fibrotic treatments. Given the prominent role of the transforming growth factor-β (TGFβ) family in fibrosis, efforts have focused on inhibiting TGFβ signalling. Despite hopes raised by the efficacy of this approach in preclinical models, translation into clinical practice has not met expectations. Antihypertensive and antidiabetic drugs slow the decline in kidney function and could slow fibrosis but, owing to the lack of technologies for in vivo renal imaging, their anti-fibrotic effect cannot be truly assessed at present. The emergence of new drugs targeting pro-fibrotic signalling, or enabling cell repair and cell metabolic reprogramming, combined with better stratification of people with CKD and the arrival of nanotechnologies for kidney-specific drug delivery, open up new perspectives for the treatment of this major public health challenge.

Indexed as

KidneyRenal Insufficiency, ChronicAnimalsFibrosisHumansTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID39934355

What OpenQuestion 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 OpenQuestion graph.