Evidence map›Paper›PMID 22278018›Full record

ArticleKidney international2012

Tubular cell dedifferentiation and peritubular inflammation are coupled by the transcription regulator Id1 in renal fibrogenesis.

Yingjian Li, Xiaoyan Wen, Youhua Liu

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. S100A1 Promotes MDM2-Mediated KLF15 Ubiquitination to Regulate ID1-Driven Tubular Injury in Diabetic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Wnt/β-catenin signaling and kidney fibrosis.Kidney international supplements · 2014
    Review
  15. Article
  16. Article
  17. Article
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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.

Yingjian LiDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
Xiaoyan Wen
Youhua Liu
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
Beta-catenin Signaling and Podocyte DysfunctionR01DK091239 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LIU, YOUHUA · 2012 to 2015
$895k
NIDDK NIH HHS DK061408NIDDK NIH HHS DK064005NIDDK NIH HHS R01 DK061408NIDDK NIH HHS R01 DK064005NIDDK NIH HHS R01 DK091239
6 · The paper itself

Abstract

During renal fibrogenesis, tubular epithelial-mesenchymal transition is closely associated with peritubular inflammation; however, it is not clear whether these two processes are connected. We previously identified the inhibitor of differentiation-1 (Id1), a dominant negative antagonist of basic helix-loop-helix transcription factors, as a major trigger of tubular cell dedifferentiation after injury. Id1 was induced selectively in degenerated proximal tubule and collecting duct epithelia after injury and was present in both the cytoplasm and nucleus, suggesting shuttling between these two compartments. Interestingly, the upregulation of Id1 was associated with peritubular inflammation in mouse and human nephropathies. In vitro, Id1 potentiated NF-κB signaling and augmented RANTES expression in kidney epithelial cells, which led to an enhanced recruitment of inflammatory cells. Id1 also induced Snail1 expression and triggered tubular epithelial dedifferentiation. In vivo, genetic ablation of Id1 in mice reduced peritubular inflammation and decreased tubular expression of RANTES following ureteral obstruction. Mice lacking Id1 were also protected against myofibroblast activation and matrix expression, leading to a reduced total collagen deposition in obstructive nephropathy. Thus, these results indicate that Id1 shuttles between nucleus and cytoplasm, and promotes peritubular inflammation and tubular epithelial dedifferentiation, suggesting that these two events are intrinsically coupled during renal fibrogenesis.

Indexed as

Cell DedifferentiationEpithelial-Mesenchymal TransitionActive Transport, Cell NucleusAnimalsCase-Control StudiesCell LineCell NucleusChemokine CCL5CollagenCytoplasmFibrosisHumansInflammation MediatorsInhibitor of Differentiation Protein 1Kidney Tubules, ProximalMiceChemokine CCL5CollagenID1 protein, humanIdb1 protein, mouseInflammation MediatorsInhibitor of Differentiation Protein 1NF-kappa BSNAI1 protein, humanSnai1 protein, mouseSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID22278018
PMCPMC3326205
OpenAlexW2087103113

What OpenQuestion holds

Textmetadata
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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.