Evidence map›Paper›PMID 22062629›Full record

ArticleFree radical biology & medicine2012

Manganese superoxide dismutase inhibits neointima formation through attenuation of migration and proliferation of vascular smooth muscle cells.

Jia-Ning Wang, Ning Shi, Shi-You Chen

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 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
2.4field-weighted citation impact, top 12% 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, 48 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Metabolic Stress.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  13. CaMKII (CaArteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  14. Smooth Muscle Cells Move With Mitochondria.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 2 countries.

Jia-Ning WangDepartment of Physiology & Pharmacology, University of Georgia, Athens, GA 30602, USA.
Ning Shi
Shi-You Chen
University of Georgia · US

Funding

Smad2 and Smooth Muscle Differentiation from Neural Crest Stem CellsR01HL093429 · NHLBI · UNIVERSITY OF GEORGIA · PI CHEN, SHIYOU · 2008 to 2013
$2.0M
Smooth Muscle Differentiation and MaturationR01HL107526 · NHLBI · UNIVERSITY OF GEORGIA · PI CHEN, SHIYOU · 2011 to 2014
$1.5M
NHLBI NIH HHS HL093429NHLBI NIH HHS HL107526NHLBI NIH HHS R01 HL093429NHLBI NIH HHS R01 HL107526
6 · The paper itself

Abstract

Superoxide anion is elevated during neointima development and is essential for neointimal vascular smooth muscle cell (VSMC) proliferation. However, little is known about the role of manganese superoxide dismutase (MnSOD, SOD2) in the neointima formation following vascular injury. SOD2 in the mitochondria plays an important role in cellular defense against oxidative damage. Because of its subcellular localization, SOD2 is considered the first line of defense against oxidative stress and plays a central role in metabolizing superoxide. Because mitochondria are the most important sources of superoxide anion, we speculated that SOD2 may have therapeutic benefits in preventing vascular remodeling. In this study, we used a rat carotid artery balloon-injury model and an adenoviral gene delivery approach to test the hypothesis that SOD2 suppresses vascular lesion formation. SOD2 was activated along with the progression of neointima formation in balloon-injured rat carotid arteries. Depletion of SOD2 by RNA interference markedly promoted the lesion formation, whereas SOD2 overexpression suppressed the injury-induced neointima formation via attenuation of migration and proliferation of VSMCs. SOD2 exerts its inhibitory effect on VSMC migration induced by angiotensin II by scavenging superoxide anion and suppressing the phosphorylation of Akt. Our data indicate that SOD2 is a negative modulator of vascular lesion formation after injury. Therefore, SOD2 augmentation may be a promising therapeutic strategy for the prevention of lesion formation in proliferative vascular diseases such as restenosis.

Indexed as

AdenoviridaeAngiotensin IIAnimalsCarotid ArteriesCarotid Artery InjuriesCatheterizationCell MovementCell ProliferationCoronary RestenosisGene Transfer TechniquesMaleMitochondriaMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaProto-Oncogene Proteins c-aktAngiotensin IIProto-Oncogene Proteins c-aktRNA, Small InterferingSuperoxide DismutaseSuperoxides

Identifiers

PMID22062629
PMCPMC3356780
OpenAlexW2085144175

What OpenQuestion holds

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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.