Evidence map›Paper›PMID 28785050›Full record

ArticleScientific reports2017

Early involvement of cellular stress and inflammatory signals in the pathogenesis of tubulointerstitial kidney disease due to UMOD mutations.

Matteo Trudu, Celine Schaeffer, Michela Riba, Masami Ikehata, Paola Brambilla, Piergiorgio Messa, Filippo Martinelli-Boneschi, Maria Pia Rastaldi, Luca Rampoldi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 44 citations in OpenAlex.

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  12. Tubulointerstitial nephritis in children and adolescents.Pediatric nephrology (Berlin, Germany) · 2025
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  18. Clinical and genetic spectra of autosomal dominant tubulointerstitial kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    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

9 authors at 3 institutions in 1 country.

Matteo TruduMolecular Genetics of Renal Disorders Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Celine SchaefferMolecular Genetics of Renal Disorders Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Michela RibaCentre for Translational Genomics and Bioinformatics, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Masami IkehataFondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, Milan, Italy.
Paola BrambillaInflammatory CNS disorders, INSPE Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Piergiorgio MessaFondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, Milan, Italy.
Filippo Martinelli-BoneschiInflammatory CNS disorders, INSPE Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Maria Pia RastaldiFondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico, Milan, Italy.
Luca RampoldiMolecular Genetics of Renal Disorders Unit, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy. rampoldi.luca@hsr.it.ORCID 0000-0002-0544-7042
Vita-Salute San Raffaele University · ITUniversity of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autosomal dominant tubulointerstitial kidney disease (ADTKD) is an inherited disorder that causes progressive kidney damage and renal failure. Mutations in the UMOD gene, encoding uromodulin, lead to ADTKD-UMOD related. Uromodulin is a GPI-anchored protein exclusively produced by epithelial cells of the thick ascending limb of Henle's loop. It is released in the tubular lumen after proteolytic cleavage and represents the most abundant protein in human urine in physiological condition. We previously generated and characterized a transgenic mouse model expressing mutant uromodulin (Tg

Indexed as

Gene Regulatory NetworksMutationAnimalsDisease Models, AnimalEndoplasmic ReticulumEndoplasmic Reticulum StressFemaleGene Expression ProfilingGene Expression RegulationHumansLipid MetabolismMaleMiceMice, TransgenicNephritis, InterstitialUromodulinUMOD protein, humanUromodulin

Identifiers

PMID28785050
PMCPMC5547146
OpenAlexW2740696525

What OpenQuestion holds

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LicenceCC BY
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.