Evidence map›Paper›PMID 37268107›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2023

EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.

Narihito Tatsumoto, Suguru Saito, Ian R Rifkin, Ramon G Bonegio, Daniel N Leal, Ganes C Sen, Moshe Arditi, Michifumi Yamashita

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

Article in Laboratory investigation; a journal of technical methods and pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
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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

8 authors at 3 institutions in 1 country.

Narihito TatsumotoDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Suguru SaitoDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Ian R RifkinRenal Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Renal Section, Department of Medicine, VA Boston Healthcare System, Boston, Massachusetts.
Ramon G BonegioRenal Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Renal Section, Department of Medicine, VA Boston Healthcare System, Boston, Massachusetts.
Daniel N LealDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California.
Ganes C SenDepartment of Inflammation & Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Moshe ArditiDivision of Infectious Diseases and Immunology, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, California; Infectious and Immunologic Diseases Research Center, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California.
Michifumi YamashitaDepartment of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: Michifumi.Yamashita@csmc.edu.
Cedars-Sinai Medical Center · USBoston University · USCleveland Clinic Lerner College of Medicine · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
TELOMERASE INACTIVATION BY RNASE L SIGNALS CELL DEATHP01CA062220 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI LI, XIAOXIA · 1994 to 2020
$35.6M
The Effect of Nanoparticle Encapsulated Resveratrol on Treatment of PeriodontitisKL2TR001882 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Elizabeta Nemeth · 2016 to 2026
$13.1M
NCATS NIH HHS KL2 TR001882NCATS NIH HHS UL1 TR001881NCI NIH HHS P01 CA062220
6 · The paper itself

Abstract

Glomerulonephritis (GN) is a group of inflammatory diseases and an important cause of morbidity and mortality worldwide. The initiation of the inflammatory process is quite different for each type of GN; however, each GN is characterized commonly and variably by acute inflammation with neutrophils and macrophages and crescent formation, leading to glomerular death. Toll-like receptor (TLR) 7 is a sensor for self-RNA and implicated in the pathogenesis of human and murine GN. Here, we show that TLR7 exacerbates glomerular injury in nephrotoxic serum nephritis (NTN), a murine model of severe crescentic GN. TLR7

Indexed as

Epidermal Growth FactorGlomerulonephritisAnimalsErbB ReceptorsHumansMacrophagesMiceToll-Like Receptor 7Epidermal Growth FactorErbB ReceptorsTLR7 protein, humanToll-Like Receptor 7crescentepidermal growth factor receptorglomerulonephritismacrophageToll-like receptor

Identifiers

PMID37268107
PMCPMC10527264
OpenAlexW4379012077

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.