Evidence map›Paper›PMID 27140856›Full record

ReviewNature reviews. Nephrology2016

Developmental signalling pathways in renal fibrosis: the roles of Notch, Wnt and Hedgehog.

Maria Edeling, Grace Ragi, Shizheng Huang, Hermann Pavenstädt, Katalin Susztak

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
248citing papers in PubMed, 2 pooled it
17.8field-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

248 citing papers in PubMed, 2 syntheses or guidelines pooled it, 414 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  10. KMT5a-Mediated IRF3 Stabilization Enhances Macrophage Chemotaxis and Renal Fibrosis Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  12. Article
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  19. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  20. Review

188 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

5 authors at 2 institutions in 2 countries.

Maria EdelingRenal Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 415 Curie Boulevard, 415 Clinical Research Building, Philadelphia, Pennsylvania 19104, USA.
Grace RagiRenal Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 415 Curie Boulevard, 415 Clinical Research Building, Philadelphia, Pennsylvania 19104, USA.
Shizheng HuangRenal Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 415 Curie Boulevard, 415 Clinical Research Building, Philadelphia, Pennsylvania 19104, USA.
Hermann PavenstädtDepartment of Molecular Nephrology, Internal Medicine D, University Hospital Albert-Schweitzer-Straße 33, Münster 48149, Germany.
Katalin SusztakRenal Electrolyte and Hypertension Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 415 Curie Boulevard, 415 Clinical Research Building, Philadelphia, Pennsylvania 19104, USA.
University of Pennsylvania · USUniversity Hospital Münster · DE

Funding

Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
APOL1 associated kidney diseaseR01DK105821 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2016 to 2024
$4.6M
Epigenetic drivers and biomarkers of diabetic kidney diseaseDP3DK108220 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2015 to 2015
$2.4M
NIDDK NIH HHS DP3 DK108220NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK105821
6 · The paper itself

Abstract

Kidney fibrosis is a common histological manifestation of functional decline in the kidney. Fibrosis is a reactive process that develops in response to excessive epithelial injury and inflammation, leading to myofibroblast activation and an accumulation of extracellular matrix. Here, we describe how three key developmental signalling pathways - Notch, Wnt and Hedgehog (Hh) - are reactivated in response to kidney injury and contribute to the fibrotic response. Although transient activation of these pathways is needed for repair of injured tissue, their sustained activation is thought to promote fibrosis. Excessive Wnt and Notch expression prohibit epithelial differentiation, whereas increased Wnt and Hh expression induce fibroblast proliferation and myofibroblastic transdifferentiation. Notch, Wnt and Hh are fundamentally different signalling pathways, but their choreographed activation seems to be just as important for fibrosis as it is for embryonic kidney development. Decreasing the activity of Notch, Wnt or Hh signalling could potentially provide a new therapeutic strategy to ameliorate the development of fibrosis in chronic kidney disease.

Indexed as

AnimalsDisease Models, AnimalFibroblastsFibrosisHedgehog ProteinsHomeostasisHumansKidneyPodocytesReceptors, NotchRenal Insufficiency, ChronicSignal TransductionWnt Signaling PathwayHedgehog ProteinsReceptors, Notch

Identifiers

PMID27140856
PMCPMC5529143
OpenAlexW2347076418

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.