Evidence map›Paper›PMID 34894725›Full record

ArticleAmerican journal of physiology. Renal physiology2022

IL-1 receptor signaling in podocytes limits susceptibility to glomerular damage.

Jiafa Ren, Xiaohan Lu, Gentzon Hall, Jamie R Privratsky, Matthew J Robson, Randy D Blakely, Steven D Crowley

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

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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

7 authors at 2 institutions in 2 countries.

Jiafa RenDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Centers, Durham, North Carolina.
Xiaohan LuDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Centers, Durham, North Carolina.
Gentzon HallDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Centers, Durham, North Carolina.
Jamie R PrivratskyDepartment of Anesthesiology, Durham Veterans Affairs and Duke University Medical Centers, Durham, North Carolina.ORCID 0000-0003-3598-4911
Matthew J RobsonDivision of Pharmaceutical Sciences, James L. Winkle College of Pharmacy, University of Cincinnati, Cincinnati, Ohio.
Randy D BlakelyDepartment of Biomedical Science, Charles E. Schmidt College of Medicine and FAU Brain Institute, Jupiter, Florida.
Steven D CrowleyDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Centers, Durham, North Carolina.
Duke Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Role of Dendritic Cell-mediated T Cell Activation in Salt-sensitive HypertensionR01HL128355 · NHLBI · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2016 to 2019
$1.9M
The interleukin-1 receptor regulates crosstalk between myeloid and renal tubular cells in hypertensionR01DK118019 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2019 to 2022
$1.7M
The Role of Interleukin-15 Receptor-alpha Variants in the Pathogenesis of FSGSK08DK111940 · NIDDK · DUKE UNIVERSITY · PI HALL, GENTZON · 2017 to 2021
$794k
The role of the M1 macrophage response in the progression of chronic kidney diseaseI01BX000893 · VA · DURHAM VA MEDICAL CENTER · PI Steven D Crowley · 2012 to 2026
–
BLRD VA I01 BX000893NHLBI NIH HHS R01 HL128355NIDDK NIH HHS K08 DK111940NIDDK NIH HHS R01 DK118019
6 · The paper itself

Abstract

Interleukin (IL)-1 receptor type 1 (IL-1R1) activation triggers a proinflammatory signaling cascade that can exacerbate kidney injury. However, the functions of podocyte IL-1R1 in glomerular disease remain unclear. To study the role of IL-1R1 signaling in podocytes, we selectively ablated podocyte IL-1R1 in mice (PKO mice). We then subjected PKO mice and wild-type controls to two glomerular injury models: nephrotoxic serum (NTS)- and adriamycin-induced nephropathy. Surprisingly, we found that IL-1R1 activation in podocytes limited albuminuria and podocyte injury during NTS- and adriamycin-induced nephropathy. Moreover, deletion of IL-1R1 in podocytes drove podocyte apoptosis and glomerular injury through diminishing Akt activation. Activation of Akt signaling abrogated the differences in albuminuria and podocyte injury between wild-type and PKO mice during NTS. Thus, IL-1R1 signaling in podocytes limits susceptibility to glomerular injury via an Akt-dependent signaling pathway. These data identify an unexpected protective role for IL-1R1 signaling in podocytes in the pathogenesis of glomerular disease.

Indexed as

AnimalsApoptosisCell LineDisease Models, AnimalDoxorubicinGlomerulonephritisHumansInterleukin-1betaIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, 129 StrainMice, KnockoutPodocytesProteinuriaProto-Oncogene Proteins c-aktDoxorubicinIL1B protein, humanIL1R1 protein, humanIL1R1 protein, mouseInterleukin-1betaIntracellular Signaling Peptides and ProteinsMembrane ProteinsNPHS2 proteinProto-Oncogene Proteins c-aktReceptors, Interleukin-1 Type Iapoptosisinterleukin-1kidneypodocyteproteinuria

Identifiers

PMID34894725
PMCPMC8782651
OpenAlexW4200314233

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.