Evidence map›Paper›PMID 22652704›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

Natriuretic peptide receptor guanylyl cyclase-A protects podocytes from aldosterone-induced glomerular injury.

Yoshihisa Ogawa, Masashi Mukoyama, Hideki Yokoi, Masato Kasahara, Kiyoshi Mori, Yukiko Kato, Takashige Kuwabara, Hirotaka Imamaki, Tomoko Kawanishi, Kenichi Koga and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Renal Tubule Cell-SpecificHypertension (Dallas, Tex. : 1979) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Podocyte cell-specificPhysiological genomics · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Osteocrin, a bone-derived humoral factor, exerts a renoprotective role in ischemia-reperfusion injury in mice.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  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

15 authors at 3 institutions in 1 country.

Yoshihisa OgawaDepartment of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Japan.
Masashi Mukoyama
Hideki Yokoi
Masato Kasahara
Kiyoshi Mori
Yukiko Kato
Takashige Kuwabara
Hirotaka Imamaki
Tomoko Kawanishi
Kenichi Koga
Akira Ishii
Takeshi Tokudome
Ichiro Kishimoto
Akira Sugawara
Kazuwa Nakao
Kyoto University · JPKyoto University of Education · JPNational Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natriuretic peptides produced by the heart in response to cardiac overload exert cardioprotective and renoprotective effects by eliciting natriuresis, reducing BP, and inhibiting cell proliferation and fibrosis. These peptides also antagonize the renin-angiotensin-aldosterone system, but whether this mechanism contributes to their renoprotective effect is unknown. Here, we examined the kidneys of mice lacking the guanylyl cyclase-A (GC-A) receptor for natriuretic peptides under conditions of high aldosterone and high dietary salt. After 4 weeks of administering aldosterone and a high-salt diet, GC-A knockout mice, but not wild-type mice, exhibited accelerated hypertension with massive proteinuria. Aldosterone-infused GC-A knockout mice had marked mesangial expansion, segmental sclerosis, severe podocyte injury, and increased oxidative stress. Reducing the BP with hydralazine failed to lessen such changes; in contrast, blockade of the renin-angiotensin-aldosterone system markedly reduced albuminuria, ameliorated podocyte injury, and reduced oxidative stress. Furthermore, treatment with the antioxidant tempol significantly reduced albuminuria and abrogated the histologic changes. In cultured podocytes, natriuretic peptides inhibited aldosterone-induced mitogen-activated protein kinase phosphorylation. Taken together, these results suggest that renoprotective properties of the endogenous natriuretic peptide/GC-A system may result from the local inhibition of the renin-angiotensin-aldosterone system and oxidative stress in podocytes.

Indexed as

Acute Kidney InjuryAldosteroneAnimalsAntihypertensive AgentsBlood PressureCells, CulturedExtracellular Signal-Regulated MAP KinasesHydralazineHypertensionMaleMiceMice, Inbred C57BLMice, KnockoutModels, AnimalOxidative Stressp38 Mitogen-Activated Protein KinasesAldosteroneAntihypertensive Agentsatrial natriuretic factor receptor AExtracellular Signal-Regulated MAP KinasesHydralazinep38 Mitogen-Activated Protein KinasesReceptors, Atrial Natriuretic FactorSodium Chloride, Dietary

Identifiers

PMID22652704
PMCPMC3380647
OpenAlexW2145738121

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.