Evidence map›Paper›PMID 23472618›Full record

ReviewAntioxidants & redox signaling2014

Oxidative stress in hypertension: role of the kidney.

Magali Araujo, Christopher S Wilcox

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 182 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Targeting NHypertension (Dallas, Tex. : 1979) · 2025
    Article
  10. Review
  11. Review
  12. Review
  13. Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
    Review
  19. Deletion ofiScience · 2024
    Article
  20. Review

46 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Magali AraujoHypertension, Kidney and Vascular Research Center, Georgetown University , Washington, District of Columbia.
Christopher S Wilcox
Georgetown University · US

Funding

Renal Vascular Oxidative Stress in HypertensionP01HL068686 · NHLBI · GEORGETOWN UNIVERSITY · PI JOSE, PEDRO A., SANDBERG, KATHRYN L · 2001 to 2017
$28.8M
REGULATION OF RENAL FUNCTION AND BP BY THROMBOXANER37DK036079 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 2003 to 2012
$5.2M
NITRIC OXIDE SYNTHASE IN THE JUXTAGLOMERULAR APPARATUSR01DK049870 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 1994 to 2014
$4.6M
REGULATION OF RENAL FUNCTION AND BP BY THROMBOXANER01DK036079 · NIDDK · UNIVERSITY OF FLORIDA · PI WILCOX, CHRISTOPHER S · 1986 to 2002
$830k
NHLBI NIH HHS P01 HL068686NIDDK NIH HHS DK-036079NIDDK NIH HHS DK-049870NIDDK NIH HHS R01 DK049870NIDDK NIH HHS R37 DK036079
6 · The paper itself

Abstract

significanceRenal oxidative stress can be a cause, a consequence, or more often a potentiating factor for hypertension. Increased reactive oxygen species (ROS) in the kidney have been reported in multiple models of hypertension and related to renal vasoconstriction and alterations of renal function. Nicotinamide adenine dinucleotide phosphate oxidase is the central source of ROS in the hypertensive kidney, but a defective antioxidant system also can contribute. RECENT ADVANCES: Superoxide has been identified as the principal ROS implicated for vascular and tubular dysfunction, but hydrogen peroxide (H2O2) has been implicated in diminishing preglomerular vascular reactivity, and promoting medullary blood flow and pressure natriuresis in hypertensive animals. CRITICAL ISSUES AND FUTURE DIRECTIONS: Increased renal ROS have been implicated in renal vasoconstriction, renin release, activation of renal afferent nerves, augmented contraction, and myogenic responses of afferent arterioles, enhanced tubuloglomerular feedback, dysfunction of glomerular cells, and proteinuria. Inhibition of ROS with antioxidants, superoxide dismutase mimetics, or blockers of the renin-angiotensin-aldosterone system or genetic deletion of one of the components of the signaling cascade often attenuates or delays the onset of hypertension and preserves the renal structure and function. Novel approaches are required to dampen the renal oxidative stress pathways to reduced O2(-•) rather than H2O2 selectivity and/or to enhance the endogenous antioxidant pathways to susceptible subjects to prevent the development and renal-damaging effects of hypertension.

Indexed as

Oxidative StressAnimalsBiological TransportHemodynamicsHumansHypertensionKidneyKidney GlomerulusKidney TubulesOxidation-ReductionReactive Oxygen SpeciesRenal CirculationRenin-Angiotensin SystemReactive Oxygen Species

Identifiers

PMID23472618
PMCPMC3880923
OpenAlexW2056024606

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.