Evidence map›Paper›PMID 20042458›Full record

ArticleAmerican journal of physiology. Renal physiology2010

Angiotensin type 2 receptor actions contribute to angiotensin type 1 receptor blocker effects on kidney fibrosis.

Takashi Naito, Li-Jun Ma, Haichun Yang, Yiqin Zuo, Yiwei Tang, Jee Young Han, Valentina Kon, Agnes B Fogo

Abstract readComparative Study
In one paragraph

Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.6field-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

38 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The Angiotensin ATPharmacological reviews · 2022
    Review
  5. Article
  6. Article
  7. Review
  8. Targeting ATAmerican journal of physiology. Renal physiology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Effects of combination PPARγ agonist and angiotensin receptor blocker on glomerulosclerosis.Laboratory investigation; a journal of technical methods and pathology · 2016
    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

8 authors at 1 institution in 1 country.

Takashi NaitoDepartment of Pathology, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2561, USA.
Li-Jun Ma
Haichun Yang
Yiqin Zuo
Yiwei Tang
Jee Young Han
Valentina Kon
Agnes B Fogo
Vanderbilt University Medical Center · US

Funding

ROLE OF SCAVENGER RECEPTORS IN RENAL FIBROSISP50DK044757 · NIDDK · VANDERBILT UNIVERSITY · PI FOGO, AGNES B. · 1992 to 2011
$11.5M
NIDDK NIH HHS DK-44757NIDDK NIH HHS DK-58942NIDDK NIH HHS P50 DK044757
6 · The paper itself

Abstract

Angiotensin type 1 (AT1) receptor blocker (ARB) ameliorates progression of chronic kidney disease. Whether this protection is due solely to blockade of AT1, or whether diversion of angiotensin II from the AT1 to the available AT2 receptor, thus potentially enhancing AT2 receptor effects, is not known. We therefore investigated the role of AT2 receptor in ARB-induced treatment effects in chronic kidney disease. Adult rats underwent 5/6 nephrectomy. Glomerulosclerosis was assessed by renal biopsy 8 wk later, and rats were divided into four groups with equivalent glomerulosclerosis: no further treatment, ARB, AT2 receptor antagonist, or combination. By week 12 after nephrectomy, systolic blood pressure was decreased in all treatment groups, but proteinuria was decreased only with ARB. Glomerulosclerosis increased significantly in AT2 receptor antagonist vs. ARB. Kidney cortical collagen content was decreased in ARB, but increased in untreated 5/6 nephrectomy, AT2 receptor antagonist, and combined groups. Glomerular cell proliferation increased in both untreated 5/6 nephrectomy and AT2 receptor antagonist vs. ARB, and phospho-Erk2 was increased by AT2 receptor antagonist. Plasminogen activator inhibitor-1 mRNA and protein were increased at 12 wk by AT2 receptor antagonist in contrast to decrease with ARB. Podocyte injury is a key component of glomerulosclerosis. We therefore assessed effects of AT1 vs. AT2 blockade on podocytes and interaction with plasminogen activator inhibitor-1. Cultured wild-type podocytes, but not plasminogen activator inhibitor-1 knockout, responded to angiotensin II with increased collagen, an effect that was completely blocked by ARB with lesser effect of AT2 receptor antagonist. We conclude that the benefical effects on glomerular injury achieved with ARB are contributed to not only by blockade of the AT1 receptor, but also by increasing angiotensin effects transduced through the AT2 receptor.

Indexed as

Angiotensin II Type 2 Receptor BlockersAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsApoptosisBlood PressureCell ProliferationCells, CulturedChronic DiseaseCollagenDisease Models, AnimalFibrinolysinFibrosisGlomerular Filtration RateImidazolesKidneyAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensin II Type 2 Receptor BlockersCollagenFibrinolysinImidazolesLosartanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PD 123319Plasminogen Activator Inhibitor 1PyridinesReceptor, Angiotensin, Type 2RNA, Messenger

Identifiers

PMID20042458
PMCPMC2838584
OpenAlexW2126508026

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.