Evidence map›Paper›PMID 18057217›Full record

ArticleJournal of the American Society of Nephrology : JASN2008

Overexpression of angiotensinogen increases tubular apoptosis in diabetes.

Fang Liu, Marie-Luise Brezniceanu, Chih-Chang Wei, Isabelle Chénier, Sébastien Sachetelli, Shao-Ling Zhang, Janos G Filep, Julie R Ingelfinger, John S D Chan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  5. Article
  6. Role of renal tubular programed cell death in diabetic kidney disease.Diabetes/metabolism research and reviews · 2023
    Review
  7. Article
  8. Review
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  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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  16. Article
  17. Insights into Diabetic Kidney Disease Using Urinary Proteomics and Bioinformatics.Journal of the American Society of Nephrology : JASN · 2017
    Review
  18. Article
  19. Article
  20. Article
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.

Fang LiuUniversité de Montréal Centre hospitalier de l'Université de Montréal-Hôtel-Dieu, Research Centre Pavillon Masson, 3850 Saint Urbain Street, Montreal, Quebec, Canada H2W 1T8.
Marie-Luise Brezniceanu
Chih-Chang Wei
Isabelle Chénier
Sébastien Sachetelli
Shao-Ling Zhang
Janos G Filep
Julie R Ingelfinger
John S D Chan
Association of Canadian College and University Teachers of English · CAHarvard University · USHôpital Maisonneuve-Rosemont · CA

Funding

ROLES OF THE PROXIMAL TUBULE RENIN ANGIOTENSIN SYSTEMR01HL048455 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI INGELFINGER, JULIE R. · 1992 to 2000
$295k
NHLBI NIH HHS HL-48455
6 · The paper itself

Abstract

The intrarenal renin-angiotensin system (RAS) plays an important role in the progression of diabetic nephropathy. We have previously reported that mice overexpressing angiotensinogen in renal proximal tubular cells (RPTC) develop hypertension, albuminuria, and renal injury. Here, we investigated whether activation of the intrarenal RAS contributes to apoptosis of RPTC in diabetes. Induction of diabetes with streptozotocin in these transgenic mice led to significant increases in BP, albuminuria, RPTC apoptosis, and proapoptotic gene expression compared with diabetic nontransgenic littermates. Insulin and/or RAS blockers markedly attenuated these changes. Hydralazine prevented hypertension but not albuminuria, RPTC apoptosis, or proapoptotic gene expression. In vitro, high-glucose medium significantly increased apoptosis and caspase-3 activity in rat immortalized RPTC overexpressing angiotensinogen compared with control cells, and these changes were prevented by insulin and/or RAS blockers. In conclusion, intrarenal RAS activation and high glucose may act in concert to increase tubular apoptosis in diabetes, independent of systemic hypertension.

Indexed as

AlbuminuriaAngiotensinogenAnimalsAntihypertensive AgentsApoptosisbcl-2-Associated X Proteinbcl-X ProteinBlood GlucoseCell Line, TransformedDiabetes Mellitus, ExperimentalDiabetic NephropathiesHydralazineHypertension, RenalHypoglycemic AgentsInsulinKidney Tubules, ProximalAngiotensinogenAntihypertensive AgentsBax protein, mousebcl-2-Associated X ProteinBcl2l1 protein, mousebcl-X ProteinBlood GlucoseHydralazineHypoglycemic AgentsInsulinLosartanPerindopril

Identifiers

PMID18057217
PMCPMC2396745
OpenAlexW2127544685

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.