Evidence map›Paper›PMID 38280906›Full record

ArticleScientific reports2024

The podocytes' inflammatory responses in experimental GN are independent of canonical MYD88-dependent toll-like receptor signaling.

Thomas Schömig, Paul Diefenhardt, Ingo Plagmann, Bastian Trinsch, Tim Merz, Giuliano Crispatzu, David Unnersjö-Jess, Jasper Nies, David Pütz, Claudio Sierra Gonzalez and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
  2. Review
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

14 authors at 3 institutions in 1 country.

Thomas SchömigDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Paul DiefenhardtDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Ingo PlagmannDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Bastian TrinschDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Tim MerzDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Giuliano CrispatzuDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
David Unnersjö-JessDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Jasper NiesDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
David PützDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Claudio Sierra GonzalezDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Bernhard SchermerDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Thomas BenzingDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany.
Paul Thomas BrinkkoetterDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany. paul.brinkkoetter@uk-koeln.de.
Sebastian BrählerDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne and University Hospital Cologne, Cologne, Germany. sebastian.braehler@uk-koeln.de.
University Hospital Cologne · DEUniversity of Cologne · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DE

Funding

Bundesministerium für Bildung und Forschung STOP-FSGS 01GM1901EDeutsche Forschungsgemeinschaft BR-2955/8Deutsche Forschungsgemeinschaft CRU329
6 · The paper itself

Abstract

Podocytes form the kidney filtration barrier and continuously adjust to external stimuli to preserve their integrity even in the presence of inflammation. It was suggested that canonical toll-like receptor signaling, mediated by the adaptor protein MYD88, plays a crucial role in initiating inflammatory responses in glomerulonephritis (GN). We explored the influence of podocyte-intrinsic MYD88 by challenging wild-type (WT) and podocyte-specific Myd88 knockout (MyD88

Indexed as

GlomerulonephritisPodocytesAdaptor Proteins, Signal TransducingAnimalsInflammationMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88ProteinuriaToll-Like ReceptorsAdaptor Proteins, Signal TransducingMyd88 protein, mouseMyeloid Differentiation Factor 88Toll-Like Receptors

Identifiers

PMID38280906
PMCPMC10821883
OpenAlexW4391277657

What OpenQuestion holds

Textmetadata
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.