Evidence map›Paper›PMID 26236989›Full record

ArticleNature medicine2015

Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease.

M Teresa Grande, Berta Sánchez-Laorden, Cristina López-Blau, Cristina A De Frutos, Agnès Boutet, Miguel Arévalo, R Grant Rowe, Stephen J Weiss, José M López-Novoa, M Angela Nieto

Erratum issuedOpen access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 456 papers.

0numbers the graph read from it
0cells of the map it votes in
456citing papers in PubMed
31.3field-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

456 citing papers in PubMed, 789 citations in OpenAlex.

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396 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

M Teresa GrandeInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Berta Sánchez-LaordenInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Cristina López-BlauInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Cristina A De FrutosInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Agnès BoutetInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Miguel ArévaloUniversity of Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
R Grant RoweDivision of Molecular Medicine and Genetics, Department of Internal Medicine, Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA.
Stephen J WeissDivision of Molecular Medicine and Genetics, Department of Internal Medicine, Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA.
José M López-NovoaUniversity of Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
M Angela NietoInstituto de Neurociencias Consejo Superior de Investigaciones Científicas and Universidad Miguel Hernández, San Juan de Alicante, Spain.
Instituto de Neurociencias · ESInstituto de Investigación Biomédica de Salamanca · ESUniversity of Michigan–Ann Arbor · USConsejo Superior de Investigaciones Científicas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progressive kidney fibrosis contributes greatly to end-stage renal failure, and no specific treatment is available to preserve organ function. During renal fibrosis, myofibroblasts accumulate in the interstitium of the kidney, leading to massive deposition of extracellular matrix and organ dysfunction. The origin of myofibroblasts is manifold, but the contribution of an epithelial-to-mesenchymal transition (EMT) undergone by renal epithelial cells during kidney fibrosis is still debated. We show that the reactivation of Snai1 (encoding snail family zinc finger 1, known as Snail1) in mouse renal epithelial cells is required for the development of fibrosis in the kidney. Damage-mediated Snail1 reactivation induces a partial EMT in tubular epithelial cells that, without directly contributing to the myofibroblast population, relays signals to the interstitium to promote myofibroblast differentiation and fibrogenesis and to sustain inflammation. We also show that Snail1-induced fibrosis can be reversed in vivo and that obstructive nephropathy can be therapeutically ameliorated in mice by targeting Snail1 expression. These results reconcile conflicting data on the role of the EMT in renal fibrosis and provide avenues for the design of novel anti-fibrotic therapies.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsFibrosisFolic AcidInflammationKidneyMaleMiceMice, Inbred C57BLRenal Insufficiency, ChronicSnail Family Transcription FactorsTranscription FactorsUreteral ObstructionFolic AcidSnai1 protein, mouseSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID26236989
OpenAlexW1215049722

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.