Evidence map›Paper›PMID 20019167›Full record

ReviewJournal of the American Society of Nephrology : JASN2010

New insights into epithelial-mesenchymal transition in kidney fibrosis.

Youhua Liu

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 409 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
409citing papers in PubMed, 1 pooled it
24.6field-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

409 citing papers in PubMed, 1 synthesis or guideline pooled it, 854 citations in OpenAlex.

  1. Pooled it
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  11. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  12. Article
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  14. Review
  15. Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  16. Article
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349 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

1 author at 1 institution in 1 country.

Youhua LiuDepartment of Pathology, University of Pittsburgh School of Medicine, S-405 Biomedical Science Tower, 200 Lothrop Street, Pittsburgh, PA 15261, USA. liuy@upmc.edu
University of Pittsburgh · US

Funding

Tenancin-C as a major component of the fibrogenic nicheR01DK064005 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TAN, RODERICK JASON · 2003 to 2021
$5.1M
HGF Gene Therapy for Chronic Renal FibrosisR01DK061408 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LIU, YOUHUA · 2002 to 2009
$1.9M
Integrin-linked Kinase and Renal Interstitial FibrosisR01DK071040 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LIU, YOUHUA · 2005 to 2008
$1.0M
NIDDK NIH HHS DK061408NIDDK NIH HHS DK064005NIDDK NIH HHS DK071040NIDDK NIH HHS R01 DK061408NIDDK NIH HHS R01 DK064005NIDDK NIH HHS R01 DK071040
6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT), a process by which differentiated epithelial cells undergo a phenotypic conversion that gives rise to the matrix-producing fibroblasts and myofibroblasts, is increasingly recognized as an integral part of tissue fibrogenesis after injury. However, the degree to which this process contributes to kidney fibrosis remains a matter of intense debate and is likely to be context-dependent. EMT is often preceded by and closely associated with chronic interstitial inflammation and could be an adaptive response of epithelial cells to a hostile or changing microenvironment. In addition to tubular epithelial cells, recent studies indicate that endothelial cells and glomerular podocytes may also undergo transition after injury. Phenotypic alteration of podocytes sets them in motion to functional impairment, resulting in proteinuria and glomerulosclerosis. Several intracellular signal transduction pathways such as TGFbeta/Smad, integrin-linked kinase (ILK) and Wnt/beta-catenin signaling are essential in controlling the process of EMT and presently are potential targets of antifibrotic therapy. This review highlights the current understanding of EMT and its underlying mechanisms to stimulate further discussion on its role, not only in the pathogenesis of renal interstitial fibrosis but also in the onset of podocyte dysfunction, proteinuria, and glomerulosclerosis.

Indexed as

Cell DifferentiationEpithelial CellsFibrosisHumansKidneyMesodermPodocytesSignal Transduction

Identifiers

PMID20019167
PMCPMC4554339
OpenAlexW2160109224

What OpenQuestion holds

Textmetadata
LicenceTDM
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.