Evidence map›Paper›PMID 21194353›Full record

ReviewAntioxidants & redox signaling2011

Regulation of endothelial function by mitochondrial reactive oxygen species.

Michael E Widlansky, David D Gutterman

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

127 citing papers in PubMed, 201 citations in OpenAlex.

  1. Trial
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  12. Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Acute Three-Dimensional Hypoxia Regulates Angiogenesis.Advanced healthcare materials · 2025
    Article
  19. Review
  20. Heliyon · 2024
    Article

67 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.

Michael E WidlanskyDepartment of Medicine, Cardiovascular Medicine Division and Department of Pharmacology, Medical College of Wisconsin , Milwaukee, Wisconsin.
David D Gutterman
Medical College of Wisconsin · US

Funding

Flow-Mediated Dilation of Human Coronary ArteriolesR01HL080704 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2006 to 2010
$1.8M
Role of Hydrogen Peroxide in the Mechanism of Flow-Induced Dilation of the Human R01HL094971 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2009 to 2012
$1.5M
Importance of Mitochondria in the Endothelial Dysfunction of Type 2 DiabetesK23HL089326 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI WIDLANSKY, MICHAEL E · 2009 to 2013
$680k
NHLBI NIH HHS HL080704NHLBI NIH HHS HL094971NHLBI NIH HHS K23 HL089326NHLBI NIH HHS K23HL089326
6 · The paper itself

Abstract

Mitochondria are well known for their central roles in ATP production, calcium homeostasis, and heme and steroid biosynthesis. However, mitochondrial reactive oxygen species (ROS), including superoxide and hydrogen peroxide, once thought to be toxic byproducts of mitochondrial physiologic activities, have recently been recognized as important cell-signaling molecules in the vascular endothelium, where their production, conversion, and destruction are highly regulated. Mitochondrial reactive oxygen species appear to regulate important vascular homeostatic functions under basal conditions in a variety of vascular beds, where, in particular, they contribute to endothelium-dependent vasodilation. On exposure to cardiovascular risk factors, endothelial mitochondria produce excessive ROS in concert with other cellular ROS sources. Mitochondrial ROS, in this setting, act as important signaling molecules activating prothrombotic and proinflammatory pathways in the vascular endothelium, a process that initially manifests itself as endothelial dysfunction and, if persistent, may lead to the development of atherosclerotic plaques. This review concentrates on emerging appreciation of the importance of mitochondrial ROS as cell-signaling molecules in the vascular endothelium under both physiologic and pathophysiologic conditions. Future potential avenues of research in this field also are discussed.

Indexed as

Oxidative StressCalciumElectron Transport Complex IElectron Transport Complex IIIEndothelium-Dependent Relaxing FactorsEndothelium, VascularHumansHydrogen PeroxideMembrane Potential, MitochondrialMitochondriaNitric OxidePeroxidasesSignal TransductionSuperoxidesCalciumElectron Transport Complex IElectron Transport Complex IIIEndothelium-Dependent Relaxing FactorsHydrogen PeroxideNitric OxidePeroxidasesSuperoxides

Identifiers

PMID21194353
PMCPMC3151425
OpenAlexW2015497750

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.