Evidence map›Paper›PMID 36932062›Full record

ReviewSignal transduction and targeted therapy2023

Kidney fibrosis: from mechanisms to therapeutic medicines.

Rongshuang Huang, Ping Fu, Liang Ma

Open access · goldFull text readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 483 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
483citing papers in PubMed, 1 pooled it
121.6field-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.

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

483 citing papers in PubMed, 1 synthesis or guideline pooled it, 598 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. GLP-1 receptor agonists-a potential therapy for chronic kidney disease?Clinical science (London, England : 1979) · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  18. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
  19. Article
  20. Review

423 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 1 institution in 1 country.

Rongshuang HuangKidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Ping FuKidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, 610041, China. Fupinghx@scu.edu.cn.ORCID 0000-0002-3061-5925
Liang MaKidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, 610041, China. Liang_m@scu.edu.cn.ORCID 0000-0001-8327-7969
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is estimated to affect 10-14% of global population. Kidney fibrosis, characterized by excessive extracellular matrix deposition leading to scarring, is a hallmark manifestation in different progressive CKD; However, at present no antifibrotic therapies against CKD exist. Kidney fibrosis is identified by tubule atrophy, interstitial chronic inflammation and fibrogenesis, glomerulosclerosis, and vascular rarefaction. Fibrotic niche, where organ fibrosis initiates, is a complex interplay between injured parenchyma (like tubular cells) and multiple non-parenchymal cell lineages (immune and mesenchymal cells) located spatially within scarring areas. Although the mechanisms of kidney fibrosis are complicated due to the kinds of cells involved, with the help of single-cell technology, many key questions have been explored, such as what kind of renal tubules are profibrotic, where myofibroblasts originate, which immune cells are involved, and how cells communicate with each other. In addition, genetics and epigenetics are deeper mechanisms that regulate kidney fibrosis. And the reversible nature of epigenetic changes including DNA methylation, RNA interference, and chromatin remodeling, gives an opportunity to stop or reverse kidney fibrosis by therapeutic strategies. More marketed (e.g., RAS blockage, SGLT2 inhibitors) have been developed to delay CKD progression in recent years. Furthermore, a better understanding of renal fibrosis is also favored to discover biomarkers of fibrotic injury. In the review, we update recent advances in the mechanism of renal fibrosis and summarize novel biomarkers and antifibrotic treatment for CKD.

Indexed as

CicatrixRenal Insufficiency, ChronicBiomarkersFibrosisHumansKidney TubulesBiomarkers

Identifiers

PMID36932062
PMCPMC10023808
OpenAlexW4327811820

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read17
identifiers read24
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.