Evidence map›Paper›PMID 22110472›Full record

ArticleExperimental diabetes research2011

Angiotensin II type II receptor deficiency accelerates the development of nephropathy in type I diabetes via oxidative stress and ACE2.

Shiao-Ying Chang, Yun-Wen Chen, Isabelle Chenier, Stella Le Minh Tran, Shao-Ling Zhang

Open access · hybridAbstract read
In one paragraph

Article in Experimental diabetes research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-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

31 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. The Angiotensin ATPharmacological reviews · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. ATDiabetologia · 2021
    Article
  8. Review
  9. Targeting ATAmerican journal of physiology. Renal physiology · 2021
    Article
  10. Review
  11. Decoding SARS-CoV-2 hijacking of host mitochondria in COVID-19 pathogenesis.American journal of physiology. Cell physiology · 2020
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Interaction of the renin angiotensin and cox systems in the kidney.Frontiers in bioscience (Scholar edition) · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. Insulin treatment attenuates renal ADAM17 and ACE2 shedding in diabetic Akita mice.American journal of physiology. Renal physiology · 2014
    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

5 authors at 2 institutions in 1 country.

Shiao-Ying ChangResearch Centre, Centre Hospitalier de l'Université de Montréal, Hôtel-Dieu, Pavillon Masson, 8-227, 3850 Saint Urbain Street, Montréal, QC, Canada.
Yun-Wen Chen
Isabelle Chenier
Stella Le Minh Tran
Shao-Ling Zhang
Université de Montréal · CACentre Hospitalier de l’Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the functional role(s) of angiotensin II (Ang II) type II receptor (AT(2)R) in type I diabetes is unknown, we hypothesized that AT(2)R is involved in decreasing the effects of type I diabetes on the kidneys. We induced diabetes with low-dose streptozotocin (STZ) in both AT(2)R knockout (AT(2)RKO) and wild-type (WT) male mice aged 12 weeks and followed them for 4 weeks. Three subgroups nondiabetic, diabetic, and insulin-treated diabetic (Rx insulin implant) were studied. Systolic blood pressure (SBP), physiological parameters, glomerular filtration rate (GFR), renal morphology, gene expression, and apoptosis were assessed. After 4 weeks of diabetes, compared to WT controls, AT(2)RKO mice clearly developed features of early diabetic nephropathy (DN), such as renal hypertrophy, tubular apoptosis, and progressive extracellular matrix (ECM) protein accumulation as well as increased GFR. AT(2)RKO mice presented hypertension unaffected by diabetes. Renal oxidative stress (measured as heme oxygenase 1 (HO-1) gene expression and reactive oxygen species (ROS) generation) and intrarenal renin angiotensin system components, such as angiotensinogen (Agt), AT(1)R, and angiotensin-converting enzyme (ACE) gene expression, were augmented whereas angiotensin-converting enzyme2 (ACE2) gene expression was decreased in renal proximal tubules (RPTs) of AT(2)RKO mice. The renal changes noted above were significantly enhanced in diabetic AT(2)RKO mice but partially attenuated in insulin-treated diabetic WT and AT(2)RKO mice. In conclusion, AT(2)R deficiency accelerates the development of DN, which appears to be mediated, at least in part, via heightened oxidative stress and ACE/ACE2 ratio in RPTs.

Indexed as

Oxidative StressAngiotensin-Converting Enzyme 2AnimalsApoptosisBlood PressureDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetic NephropathiesKidneyMaleMiceMice, KnockoutPeptidyl-Dipeptidase AReactive Oxygen SpeciesReceptor, Angiotensin, Type 2Renin-Angiotensin SystemAce2 protein, mouseAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AReactive Oxygen SpeciesReceptor, Angiotensin, Type 2

Identifiers

PMID22110472
PMCPMC3205615
OpenAlexW2123155343

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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.