Evidence map›Paper›PMID 24981817›Full record

ReviewNature reviews. Nephrology2014

Inflammatory processes in renal 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, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05285878 (A Phase 2, Randomized, Placebo-Controlled Study to Evaluate Fingolimod for the Abrogation of Interstitial Fibrosis and Tubular Atrophy Following Kidney Transplantation), which is not on this map. Cited by 396 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
396citing papers in PubMed, 2 pooled it
21.7field-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.

NCT05285878 phase2enrolling by invitationnot on this mapstarted 2022, after this paper: background citation

A Phase 2, Randomized, Placebo-Controlled Study to Evaluate Fingolimod for the Abrogation of Interstitial Fibrosis and Tubular Atrophy Following Kidney Transplantation

TypeinterventionalSponsorThe Methodist Hospital Research InstituteRan2022 to 2027Enrolled20ConditionsInterstitial Fibrosis, Kidney Transplant, Complications, Kidney Transplant RejectionArmsFingolimod, Placebo
3 · Its place in the literature

Who cites it

396 citing papers in PubMed, 2 syntheses or guidelines pooled it, 669 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Endothelial cell-specific knockout of ATG5 ameliorates inflammation and renal fibrosis by regulating pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  13. Article
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  15. Plants (Basel, Switzerland) · 2026
    Article
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  17. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
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  20. Review

336 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 3 countries.

Xiao-Ming MengSchool of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.
David J Nikolic-PatersonMonash University Department of Medicine, 246 Clayton Road, Clayton, Melbourne, Vic 3168, Australia.
Hui Yao LanLi Ka Shing Institute of Health Sciences and Department of Medicine &Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong.
Anhui Medical University · CNChinese University of Hong Kong · HKMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many types of kidney injury induce inflammation as a protective response. However, unresolved inflammation promotes progressive renal fibrosis, which can culminate in end-stage renal disease. Kidney inflammation involves cells of the immune system as well as activation of intrinsic renal cells, with the consequent production and release of profibrotic cytokines and growth factors that drive the fibrotic process. In glomerular diseases, the development of glomerular inflammation precedes interstitial fibrosis; although the mechanisms linking these events are poorly understood, an important role for tubular epithelial cells in mediating this link is gaining support. Data have implicated macrophages in promoting both glomerular and interstitial fibrosis, whereas limited evidence suggests that CD4(+) T cells and mast cells are involved in interstitial fibrosis. However, macrophages can also promote renal repair when the cause of renal injury can be resolved, highlighting their plasticity. Understanding the mechanisms by which inflammation drives renal fibrosis is necessary to facilitate the development of therapeutics to halt the progression of chronic kidney disease.

Indexed as

BiomarkersCD4-Positive T-LymphocytesDendritic CellsDisease ProgressionFibrosisHumansInflammationKidneyKidney DiseasesMacrophagesBiomarkers

Identifiers

PMID24981817
OpenAlexW2087627594

What OpenQuestion 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 OpenQuestion graph.