Evidence map›Paper›PMID 21473702›Full record

ReviewAntioxidants & redox signaling2011

Superoxide dismutases: role in redox signaling, vascular function, and diseases.

Tohru Fukai, Masuko Ushio-Fukai

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 900 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
900citing papers in PubMed, 1 pooled it
44.6field-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

900 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,925 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

840 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.

Tohru FukaiSection of Cardiology, Department of Medicine, University of Illinois at Chicago, 835 S. Wolcott, Chicago, IL 60612, USA. tfukai@uic.edu
Masuko Ushio-Fukai
University of Illinois Chicago · US

Funding

Vascular Extracellular Superoxide Dismutase ModulationR01HL070187 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKAI, TOHRU · 2002 to 2017
$4.2M
Reactive Oxygen Species and Endothelial MigrationR01HL077524 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI USHIO-FUKAI, MASUKO · 2006 to 2010
$2.2M
NHLBI NIH HHS R01 HL070187NHLBI NIH HHS R01 HL077524
6 · The paper itself

Abstract

Excessive reactive oxygen species Revised abstract, especially superoxide anion (O₂•-), play important roles in the pathogenesis of many cardiovascular diseases, including hypertension and atherosclerosis. Superoxide dismutases (SODs) are the major antioxidant defense systems against (O₂•-), which consist of three isoforms of SOD in mammals: the cytoplasmic Cu/ZnSOD (SOD1), the mitochondrial MnSOD (SOD2), and the extracellular Cu/ZnSOD (SOD3), all of which require catalytic metal (Cu or Mn) for their activation. Recent evidence suggests that in each subcellular location, SODs catalyze the conversion of (O₂•-), H2O2, which may participate in cell signaling. In addition, SODs play a critical role in inhibiting oxidative inactivation of nitric oxide, thereby preventing peroxynitrite formation and endothelial and mitochondrial dysfunction. The importance of each SOD isoform is further illustrated by studies from the use of genetically altered mice and viral-mediated gene transfer. Given the essential role of SODs in cardiovascular disease, the concept of antioxidant therapies, that is, reinforcement of endogenous antioxidant defenses to more effectively protect against oxidative stress, is of substantial interest. However, the clinical evidence remains controversial. In this review, we will update the role of each SOD in vascular biologies, physiologies, and pathophysiologies such as atherosclerosis, hypertension, and angiogenesis. Because of the importance of metal cofactors in the activity of SODs, we will also discuss how each SOD obtains catalytic metal in the active sites. Finally, we will discuss the development of future SOD-dependent therapeutic strategies.

Indexed as

AnimalsAtherosclerosisBlood VesselsCopperEnzyme ActivationHumansHydrogen PeroxideHypertensionManganeseMiceMolecular ChaperonesNeovascularization, PhysiologicNitric OxideOxidation-ReductionSignal TransductionSuperoxide DismutaseCopperHydrogen PeroxideManganeseMolecular ChaperonesNitric OxideSuperoxide DismutaseSuperoxides

Identifiers

PMID21473702
PMCPMC3151424
OpenAlexW1965891907

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.