Evidence map›Paper›PMID 37579299›Full record

ArticleDiabetes2023

GPR56 Promotes Diabetic Kidney Disease Through eNOS Regulation in Glomerular Endothelial Cells.

Jinshan Wu, Zhihong Wang, Minchao Cai, Xuan Wang, Benjamin Lo, Qifu Li, John Cijiang He, Kyung Lee, Jia Fu

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Novel Insights into Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  13. LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Jinshan WuDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Zhihong WangDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Minchao CaiDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Xuan WangDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Benjamin LoDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Qifu LiDepartment of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
John Cijiang HeDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.ORCID 0000-0002-1502-2849
Kyung LeeDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.ORCID 0000-0002-9756-1765
Jia FuDepartment of Medicine, Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, NY.
Icahn School of Medicine at Mount Sinai · USThe Affiliated Yongchuan Hospital of Chongqing Medical University · CNJames J. Peters VA Medical Center · US

Funding

VIRAL PATHOGENESIS OF HIV ASSOCIATED NEPHROPATHYP01DK056492 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI WYATT, CHRISTINA M · 1999 to 2021
$27.8M
The role of Vpr-mediated cell cycle dysregulation in HIV-associated kidney diseaseR01DK133912 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI John Cijiang He, Mary E. Klotman · 2022 to 2026
$3.7M
Role of RTN1A in the Progression of Diabetic NephropathyR01DK109683 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2016 to 2023
$3.3M
PP2A as a drug target for diabetic kidney diseaseR01DK122980 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG, LIU, RUIJIE · 2020 to 2024
$2.9M
The Role of LRG1 in Diabetic Kidney DiseaseR01DK117913 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Bhaskar Chandra Das, Kyung Lee · 2018 to 2026
$2.6M
Role of RARRES1 in diabetic kidney diseaseR01DK129467 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG, LEE, KYUNG · 2021 to 2024
$1.8M
Role of GPR56 in glomerular endothelial cell injury in early diabetic kidney diseaseK01DK125614 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FU, JIA · 2021 to 2025
$696k
BLRD VA I01 BX000345NIDDK NIH HHS K01 DK125614NIDDK NIH HHS P01 DK056492NIDDK NIH HHS R01 DK109683NIDDK NIH HHS R01 DK117913NIDDK NIH HHS R01 DK122980NIDDK NIH HHS R01 DK129467NIDDK NIH HHS R01 DK133912
6 · The paper itself

Abstract

Although glomerular endothelial dysfunction is well recognized as contributing to the pathogenesis of diabetic kidney disease (DKD), the molecular pathways contributing to DKD pathogenesis in glomerular endothelial cells (GECs) are only partially understood. To uncover pathways that are differentially regulated in early DKD that may contribute to disease pathogenesis, we recently conducted a transcriptomic analysis of isolated GECs from diabetic NOS3-null mice. The analysis identified several potential mediators of early DKD pathogenesis, one of which encoded an adhesion G protein-coupled receptor-56 (GPR56), also known as ADGRG1. Enhanced glomerular expression of GPR56 was observed in human diabetic kidneys, which was negatively associated with kidney function. Using cultured mouse GECs, we observed that GPR56 expression was induced with exposure to advanced glycation end products, as well as in high-glucose conditions, and its overexpression resulted in decreased phosphorylation and expression of endothelial nitric oxide synthase (eNOS). This effect on eNOS by GPR56 was mediated by coupling of Gα12/13-RhoA pathway activation and Gαi-mediated cAMP/PKA pathway inhibition. The loss of GPR56 in mice led to a significant reduction in diabetes-induced albuminuria and glomerular injury, which was associated with reduced oxidative stress and restoration of eNOS expression in GECs. These findings suggest that GPR56 promotes DKD progression mediated, in part, through enhancing glomerular endothelial injury and dysfunction. ARTICLE HIGHLIGHTS:

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesAnimalsEndothelial CellsHumansMiceNitric Oxide Synthase Type IIIReceptors, G-Protein-CoupledADGRG1 protein, humanAdgrg1 protein, mouseNitric Oxide Synthase Type IIINOS3 protein, humanNos3 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID37579299
PMCPMC10588296
OpenAlexW4385802933

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.