Evidence map›Paper›PMID 30132346›Full record

ArticleAmerican journal of physiology. Renal physiology2018

Deletion of the formin Diaph1 protects from structural and functional abnormalities in the murine diabetic kidney.

Michaele B Manigrasso, Richard A Friedman, Ravichandran Ramasamy, Vivette D'Agati, Ann Marie Schmidt

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

Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  4. Mechanistic underpinnings of AGEs-RAGE via DIAPH1 in ischemic, diabetic, and failing hearts.American journal of physiology. Heart and circulatory physiology · 2025
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  17. FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes.Journal of the American Society of Nephrology : JASN · 2020
    Article
  18. 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

5 authors at 3 institutions in 1 country.

Michaele B ManigrassoDiabetes Research Program, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, New York University School of Medicine , New York, New York.
Richard A FriedmanBiomedical Informatics Shared Resource, Herbert Irving Comprehensive Cancer Center, and Department of Biomedical Informatics, Columbia University Irving Medical Center , New York, New York.
Ravichandran RamasamyDiabetes Research Program, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, New York University School of Medicine , New York, New York.
Vivette D'AgatiDepartment of Pathology, College of Physicians and Surgeons, Columbia University , New York, New York.
Ann Marie SchmidtDiabetes Research Program, Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, New York University School of Medicine , New York, New York.
New York University · USColumbia University · USColumbia University Irving Medical Center · US

Funding

Targeting RAGE-mDia1 in Diabetic Complications: Mechanisms and TherapeuticsR24DK103032 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 2014 to 2018
$4.2M
Sandy Recovery Ventana Medical Systems Discovery XTS10OD018338 · OD · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CHIRIBOGA, LUIS A · 2014 to 2014
$123k
NIDDK NIH HHS R24 DK103032NIH HHS S10 OD018338
6 · The paper itself

Abstract

Diaphanous 1 (DIAPH1), a member of the formin family, binds to the cytoplasmic domain of the receptor for advanced glycation end products (RAGE) and is required for RAGE signal transduction. Experiments employing genetic overexpression or deletion of Ager (the gene encoding RAGE) or its pharmacological antagonism implicate RAGE in the pathogenesis of diabetes-associated nephropathy. We hypothesized that DIAPH1 contributes to pathological and functional derangements in the kidneys of diabetic mice. We show that DIAPH1 is expressed in the human and murine diabetic kidney, at least in part in the tubulointerstitium and glomerular epithelial cells or podocytes. To test the premise that DIAPH1 is linked to diabetes-associated derangements in the kidney, we rendered male mice globally devoid of Diaph1 ( Diaph1

Indexed as

Adaptor Proteins, Signal TransducingAlbuminuriaAnimalsCarrier ProteinsCase-Control StudiesCD36 AntigensCell Cycle ProteinsDiabetes Mellitus, ExperimentalDiabetic NephropathiesForminsGene DeletionGPI-Linked ProteinsHumansKidneyMaleMice, Inbred C57BLAdaptor Proteins, Signal TransducingAger protein, mouseCarrier ProteinsCD36 AntigensCd36 protein, mouseCell Cycle ProteinsDiap1 protein, mouseDIAPH1 protein, humanForminsGas1 protein, mouseGPI-Linked ProteinsNes protein, mouseNestinReceptor for Advanced Glycation End ProductsStreptozocinDIAPH1glycationkidneypodocyteRAGE

Identifiers

PMID30132346
PMCPMC6336994
OpenAlexW2888707342

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.