Evidence mapPaperPMID 22443458Full record

ReviewAntioxidants & redox signaling2013

Angiotensin II-induced production of mitochondrial reactive oxygen species: potential mechanisms and relevance for cardiovascular disease.

Sergey I Dikalov, Rafal R Nazarewicz

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 3 pooled it
6.6field-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

188 citing papers in PubMed, 3 syntheses or guidelines pooled it, 341 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Beyond the guidelines: Vascular function as the central determinant and therapeutic target in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Unlocking Novel Therapeutic Potential of Angiotensin II Receptor Blockers.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

128 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.

Sergey I DikalovFree Radicals in Medicine Core, Division of Clinical Pharmacology, Vanderbilt University Medical Center , Nashville, Tennessee.
Rafal R Nazarewicz
Vanderbilt University Medical Center · US

Funding

Mitochondrial Oxidative Stress In Angiotensis II Induced Endothelial DysfunctionR01HL094469 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 2010 to 2013
$1.6M
NHLBI NIH HHS HL094469NHLBI NIH HHS R01 HL094469
6 · The paper itself

Abstract

significanceThe role of reactive oxygen species (ROS) in angiotensin II (AngII) induced endothelial dysfunction, cardiovascular and renal remodeling, inflammation, and fibrosis has been well documented. The molecular mechanisms of AngII pathophysiological activity involve the stimulation of NADPH oxidases, which produce superoxide and hydrogen peroxide. AngII also increases the production of mitochondrial ROS, while the inhibition of AngII improves mitochondrial function; however, the specific molecular mechanisms of the stimulation of mitochondrial ROS is not clear. RECENT ADVANCES: Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases. CRITICAL ISSUES: Although mitochondrial ROS plays an important role in normal physiological cell signaling, AngII, high glucose, high fat, or hypoxia may cause the overproduction of mitochondrial ROS, leading to the feed-forward redox stimulation of NADPH oxidases. This vicious cycle may contribute to the development of pathological conditions and facilitate organ damage in hypertension, atherosclerosis, and diabetes. FUTURE DIRECTIONS: The development of antioxidant strategies specifically targeting mitochondria could be therapeutically beneficial in these disease conditions.

Indexed as

Angiotensin IIAnimalsCardiovascular DiseasesHumansHydrogen PeroxideMitochondriaNADPH OxidasesOxidative StressReactive Oxygen SpeciesSignal TransductionSuperoxide DismutaseAngiotensin IIHydrogen PeroxideNADPH OxidasesReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID22443458
PMCPMC3771548
OpenAlexW2085076776

What Socratic 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 Socratic graph.