Evidence map›Paper›PMID 23583330›Full record

ReviewFree radical biology & medicine2013

Redox signaling in cardiovascular health and disease.

Nageswara R Madamanchi, Marschall S Runge

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 2 pooled it
10.5field-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

113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Aging-AssociatedJournal of the American Heart Association · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
  12. Article
  13. Gut microbiota-mediated cardiovascular effects ofFrontiers in microbiology · 2026
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

53 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.

Nageswara R MadamanchiMcAllister Heart Institute, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: nrmadama@med.unc.edu.
Marschall S RungeMcAllister Heart Institute, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: marschall_runge@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

UNC Clinical and Translational Science AwardUL1TR000083 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUNGE, MARSCHALL S. · 2012 to 2013
$11.6M
OXIDATIVE STRESS AND VASCULAR AGINGP01AG024282 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMYTH, SUSAN S. · 2004 to 2008
$7.4M
Molecular Characterization of NoxA1 in VSMC NADPH Oxidase ActivationR01HL111664 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI RUNGE, MARSCHALL S. · 2012 to 2015
$1.5M
NCATS NIH HHS TR000083NCATS NIH HHS UL1 TR000083NHLBI NIH HHS HL111664NHLBI NIH HHS R01 HL111664NIA NIH HHS AG024282NIA NIH HHS P01 AG024282
6 · The paper itself

Abstract

Spatiotemporal regulation of the activity of a vast array of intracellular proteins and signaling pathways by reactive oxygen species (ROS) governs normal cardiovascular function. However, data from experimental and animal studies strongly support that dysregulated redox signaling, resulting from hyperactivation of various cellular oxidases or mitochondrial dysfunction, is integral to the pathogenesis and progression of cardiovascular disease (CVD). In this review, we address how redox signaling modulates the protein function, the various sources of increased oxidative stress in CVD, and the labyrinth of redox-sensitive molecular mechanisms involved in the development of atherosclerosis, hypertension, cardiac hypertrophy and heart failure, and ischemia-reperfusion injury. Advances in redox biology and pharmacology for inhibiting ROS production in specific cell types and subcellular organelles combined with the development of nanotechnology-based new in vivo imaging systems and targeted drug delivery mechanisms may enable fine-tuning of redox signaling for the treatment and prevention of CVD.

Indexed as

AnimalsCardiovascular DiseasesCardiovascular SystemHumansMitochondriaOxidation-ReductionProtein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Reactive Oxygen SpeciesTranscription FactorsProtein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanReactive Oxygen SpeciesTranscription FactorsAtherosclerosisEndothelial dysfunctionFree radicalsMitochondriaNADPH oxidasesReactive oxygen species

Identifiers

PMID23583330
PMCPMC3883979
OpenAlexW2082033913

What OpenQuestion holds

Textmetadata
LicenceTDM
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.