Evidence map›Paper›PMID 25422468›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic nephropathy.

Tony Jourdan, Gergő Szanda, Avi Z Rosenberg, Joseph Tam, Brian James Earley, Grzegorz Godlewski, Resat Cinar, Ziyi Liu, Jie Liu, Cynthia Ju and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Chemical Probes for Investigating the Endocannabinoid System.Current topics in behavioral neurosciences · 2026
    Review
  8. Article
  9. Adolescent exposure to Δ9-tetrahydrocannabinol impairs testicular function in young adult male mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  10. Article
  11. The effects of Cannabidiol on podocytes in vitro.Biochemical and biophysical research communications · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Maladaptive Peripheral Ketogenesis in Schwann Cells Mediated by CBAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  16. The effects of cannabinoids on the kidney.Acta physiologica (Oxford, England) · 2024
    Review
  17. Article
  18. The cannabinoid CBJournal of receptor and signal transduction research · 2024
    Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Tony JourdanLaboratory of Physiologic Studies, Section on Neuroendocrinology, and jourdant@mail.nih.gov george.kunos@nih.gov.
Gergő SzandaLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Avi Z RosenbergKidney Diseases Section, National Institute on Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892; The Johns Hopkins University School of Medicine, Baltimore, MD 21205; and.
Joseph TamLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Brian James EarleyLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Grzegorz GodlewskiLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Resat CinarLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Ziyi LiuLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Jie LiuLaboratory of Physiologic Studies, Section on Neuroendocrinology, and.
Cynthia JuSkaggs School of Pharmacy and Pharmaceutical Sciences, Department of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045.
Pál PacherSection on Oxidative Stress and Tissue Injury, Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism.
George KunosLaboratory of Physiologic Studies, Section on Neuroendocrinology, and jourdant@mail.nih.gov george.kunos@nih.gov.
National Institute on Alcohol Abuse and Alcoholism · USNational Institutes of Health · USUniversity of Montana · US

Funding

Endocannabinoids And Energy HomeostasisZIAAA000350 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI KUNOS, GEORGE · 2009 to 2025
$28.4M
Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Diabetic nephropathy is a major cause of end-stage kidney disease, and overactivity of the endocannabinoid/cannabinoid 1 receptor (CB1R) system contributes to diabetes and its complications. Zucker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with albuminuria, reduced glomerular filtration, activation of the renin-angiotensin system (RAS), oxidative/nitrative stress, podocyte loss, and increased CB1R expression in glomeruli. Peripheral CB1R blockade initiated in the prediabetic stage prevented these changes or reversed them when animals with fully developed diabetic nephropathy were treated. Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Agtr1) antagonist, attenuated the development of nephropathy and down-regulated renal cortical CB1R expression, without affecting the marked hyperglycemia. In cultured human podocytes, CB1R and desmin gene expression were increased and podocin and nephrin content were decreased by either the CB1R agonist arachydonoyl-2'-chloroethylamide, angiotensin II, or high glucose, and the effects of all three were antagonized by CB1R blockade or siRNA-mediated knockdown of CNR1 (the cannabinoid type 1 receptor gene). We conclude that increased CB1R signaling in podocytes contributes to the development of diabetic nephropathy and represents a common pathway through which both hyperglycemia and increased RAS activity exert their deleterious effects, highlighting the therapeutic potential of peripheral CB1R blockade.

Indexed as

Models, BiologicalAnalysis of VarianceAngiotensin IIAnimalsArachidonic AcidsDesminDiabetes Mellitus, Type 2Diabetic NephropathiesGene Expression RegulationLosartanPodocytesPyrazolesRatsRats, ZuckerReceptor, Angiotensin, Type 1Receptor, Cannabinoid, CB1Agtr1a protein, ratAngiotensin IIArachidonic Acidsarachidonyl-2-chloroethylamideDesminJD5037LosartanPyrazolesReceptor, Angiotensin, Type 1Receptor, Cannabinoid, CB1RNA, Small InterferingSulfonamidesangiotensin IIendocannabinoidhyperglycemianephropathypodocyte

Identifiers

PMID25422468
PMCPMC4273328
OpenAlexW2028879462

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.