Evidence map›Paper›PMID 22875785›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Angiotensin II stimulates superoxide production in the thick ascending limb by activating NOX4.

Katherine J Massey, Nancy J Hong, Jeffrey L Garvin

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. 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
6.4field-weighted citation impact, top 3% 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, 46 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Hydrogen peroxide (HScientific reports · 2021
    Article
  7. Article
  8. Review
  9. Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019
    Review
  10. Review
  11. Article
  12. NADPH Oxidases and Mitochondria in Vascular Senescence.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Oxidative stress and prostatic diseases.Molecular and clinical oncology · 2017
    Article
  15. Review
  16. Diabetes and Kidney Disease: Role of Oxidative Stress.Antioxidants & redox signaling · 2016
    Review
  17. Article
  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

3 authors at 1 institution in 1 country.

Katherine J MasseyHypertension and Vascular Research Division, Dept. of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA. kmassey1@hfhs.org
Nancy J Hong
Jeffrey L Garvin
Henry Ford Hospital · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI ORTIZ, PABLO A. · 1985 to 2017
$39.8M
Tubuloglomerular Feedback Regulation by Carbon MonoxideP01HL090550 · NHLBI · HENRY FORD HEALTH SYSTEM · PI ORTIZ, PABLO A. · 2009 to 2013
$10.2M
Salt-Sensitive Hypertension: Role of Renal SuperoxideR01HL070985 · NHLBI · HENRY FORD HEALTH SYSTEM · PI Jeffrey L. Garvin · 2002 to 2026
$6.3M
NHLBI NIH HHS 1P01-HL-090550-03NHLBI NIH HHS 5P01-HL-028982-30NHLBI NIH HHS 5R01-HL-070985-09NHLBI NIH HHS R01 HL070985
6 · The paper itself

Abstract

Angiotensin II (ANG II) stimulates production of superoxide (O(2)(-)) by NADPH oxidase (NOX) in medullary thick ascending limbs (TALs). There are three isoforms of the catalytic subunit (NOX1, 2, and 4) known to be expressed in the kidney. We hypothesized that NOX2 mediates ANG II-induced O(2)(-) production by TALs. To test this, we measured NOX1, 2, and 4 mRNA and protein by RT-PCR and Western blot in TAL suspensions from rats and found three catalytic subunits expressed in the TAL. We measured O(2)(-) production using a lucigenin-based assay. To assess the contribution of NOX2, we measured ANG II-induced O(2)(-) production in wild-type and NOX2 knockout mice (KO). ANG II increased O(2)(-) production by 346 relative light units (RLU)/mg protein in the wild-type mice (n = 9; P < 0.0007 vs. control). In the knockout mice, ANG II increased O(2)(-) production by 290 RLU/mg protein (n = 9; P < 0.007 vs. control). This suggests that NOX2 does not contribute to ANG II-induced O(2)(-) production (P < 0.6 WT vs. KO). To test whether NOX4 mediates the effect of ANG II, we selectively decreased NOX4 expression in rats using an adenovirus that expresses NOX4 short hairpin (sh)RNA. Six to seven days after in vivo transduction of the kidney outer medulla, NOX4 mRNA was reduced by 77%, while NOX1 and NOX2 mRNA was unaffected. In control TALs, ANG II stimulated O(2)(-) production by 96%. In TALs transduced with NOX4 shRNA, ANG II-stimulated O(2)(-) production was not significantly different from the baseline. We concluded that NOX4 is the main catalytic isoform of NADPH oxidase that contributes to ANG II-stimulated O(2)(-) production by TALs.

Indexed as

Angiotensin IIAnimalsCatalysisIsoenzymesLoop of HenleMaleMiceMice, KnockoutNADPH Oxidase 4NADPH OxidasesRatsRats, Sprague-DawleyAngiotensin IIIsoenzymesNADPH Oxidase 4NADPH OxidasesNox4 protein, rat

Identifiers

PMID22875785
PMCPMC3469600
OpenAlexW2022974361

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.