Evidence map›Paper›PMID 38671844›Full record

ArticleAntioxidants (Basel, Switzerland)2024

Endothelial NOX5 Obliterates the Reno-Protective Effect of Nox4 Deletion by Promoting Renal Fibrosis via Activation of EMT and ROS-Sensitive Pathways in Diabetes.

Karin A M Jandeleit-Dahm, Haritha R Kankanamalage, Aozhi Dai, Jaroslawna Meister, Sara Lopez-Trevino, Mark E Cooper, Rhian M Touyz, Christopher R J Kennedy, Jay C Jha

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 10 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

9 authors at 4 institutions in 3 countries.

Karin A M Jandeleit-DahmDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.
Haritha R KankanamalageDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.
Aozhi DaiDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.
Jaroslawna MeisterInstitute for Clinical Diabetology, German Diabetes Centre, Leibniz Centre for Diabetes Research at Heinrich Heine University, 40225 Düsseldorf, Germany.ORCID 0000-0003-4634-1815
Sara Lopez-TrevinoDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.
Mark E CooperDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.
Rhian M TouyzResearch Institute of the McGill University Health Centre, McGill University, Montreal, QC H3H 2R9, Canada.ORCID 0000-0003-0670-0887
Christopher R J KennedyDepartment of Medicine, Kidney Research Centre, Ottawa Hospital Research Institute, Ottawa, ON K1Y 4E9, Canada.
Jay C JhaDepartment of Diabetes, School of Translational Medicine, Monash University, Alfred Medical Research & Education Precinct, Melbourne, VIC 3004, Australia.ORCID 0000-0002-2764-2930
Monash University · AUDeutsches Diabetes-Zentrum e.V. · DEMcGill University Health Centre · CAOttawa Hospital · CA

Funding

Juvenile Diabetes Research Foundation 2-SRA 2014-259-Q-R
6 · The paper itself

Abstract

Chronic hyperglycemia induces intrarenal oxidative stress due to the excessive production of reactive oxygen species (ROS), leading to a cascade of events that contribute to the development and progression of diabetic kidney disease (DKD). NOX5, a pro-oxidant NADPH oxidase isoform, has been identified as a significant contributor to renal ROS in humans. Elevated levels of renal ROS contribute to endothelial cell dysfunction and associated inflammation, causing increased endothelial permeability, which can disrupt the renal ecosystem, leading to progressive albuminuria and renal fibrosis in DKD. This study specifically examines the contribution of endothelial cell-specific human

Indexed as

diabetic kidney diseasefibrosisinflammationNOX4NOX5reactive oxygen species (ROS)

Identifiers

PMID38671844
PMCPMC11047703
OpenAlexW4393188633

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.