Evidence map›Paper›PMID 30545984›Full record

ArticleJournal of the American Society of Nephrology : JASN2019

Expression Profiling of Fibroblasts in Chronic and Acute Disease Models Reveals Novel Pathways in Kidney Fibrosis.

Atsuko Y Higashi, Bruce J Aronow, Gregory R Dressler

Abstract readComparative Study
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Journal of translational internal medicine · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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 at 2 institutions in 1 country.

Atsuko Y HigashiDepartment of Pathology, University of Michigan, Ann Arbor, Michigan; and.
Bruce J AronowDepartment of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
Gregory R DresslerDepartment of Pathology, University of Michigan, Ann Arbor, Michigan; and dressler@umich.edu.
University of Michigan–Ann Arbor · USCincinnati Children's Hospital Medical Center · US

Funding

Research Supplement to Promote Diversity in Health Related ResearchR01DK054740 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DRESSLER, GREGORY R · 1999 to 2024
$9.0M
Epigenetic Regulation of Kidney DevelopmentR01DK073722 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DRESSLER, GREGORY R · 2006 to 2020
$4.6M
NIDDK NIH HHS R01 DK054740NIDDK NIH HHS R01 DK073722
6 · The paper itself

Abstract

backgroundRenal interstitial fibrosis results from activation and proliferation of fibroblasts to myofibroblasts, secretion and accumulation of extracellular matrix, and displacement of normal renal tubules. In contrast to chronic renal disease, acute injury may be repaired, a process that includes a decrease in the number of myofibroblasts in the interstitium and degradation of the accumulated extracellular matrix, leaving little evidence of prior injury.

methodsTo investigate whether activated fibroblasts demonstrate changes in gene expression that correspond with regression after acute injury but are not observed in chronic models of fibrosis, we used microarrays to analyze gene expression patterns among fibroblast populations at different stages of injury or repair. We then mined the data for signaling pathways in fibroblasts corresponding to the acute proliferative, regression, and chronic phases of renal injury.

resultsWe identified multiple gene clusters with changes that correlate with the three phases of renal injury, including changes in levels of receptors for the antifibrotic factor PGE2. In adult renal fibroblast cultures, PGE2 was able to upregulate many genes that are suppressed by the profibrotic cytokine TGF-

conclusionsInherent gene expression changes in activated fibroblasts accompany the transition from AKI to repair and regeneration. In chronic models, however, activated fibroblasts are resistant to the antifibrotic effects of PGE2 due to suppression of a subset of PGE receptors.

Indexed as

Gene Expression RegulationAcute Kidney InjuryAnimalsCell DifferentiationCells, CulturedDinoprostoneDisease Models, AnimalExtracellular MatrixFibroblastsFibrosisGene Expression ProfilingImmunohistochemistryMiceMyofibroblastsReal-Time Polymerase Chain ReactionRenal Insufficiency, ChronicDinoprostoneacute renal failurechronic kidney diseasefibrosismyofibroblastsprostaglandins

Identifiers

PMID30545984
PMCPMC6317603
OpenAlexW2905110158

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.