Evidence map›Paper›PMID 19751821›Full record

ReviewFree radical biology & medicine2009

Oxidative risk for atherothrombotic cardiovascular disease.

Jane A Leopold, Joseph Loscalzo

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
7.1field-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

85 citing papers in PubMed, 218 citations in OpenAlex.

  1. Trial
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  11. Antioxidants: a comprehensive review.Archives of toxicology · 2025
    Review
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  13. Review
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  16. Review
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  19. Unbalanced Redox With Autophagy in Cardiovascular Disease.Journal of lipid and atherosclerosis · 2023
    Review
  20. Article

25 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 2 institutions in 1 country.

Jane A LeopoldBrigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Joseph Loscalzo
Brigham and Women's Hospital · USHarvard University · US

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2005 to 2015
$21.5M
Single Molecule Analysis of Sickle Erythrocyte Adhesion in Sickle Cell DiseaseU54HL070819 · NHLBI · BOSTON MEDICAL CENTER · PI STEINBERG, MARTIN H. · 2003 to 2011
$12.5M
GPx-3 and Peroxide Flux in the Endothelial CellR37HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 2007 to 2016
$4.3M
Effects of Dietary Fat on Contractile and Mitochondrial Function in Heart FailureR01HL081857 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI CHANDLER, MARGARET P · 2006 to 2010
$2.2M
PLATELET DERIVED REACTIVE OXYGEN SPECIES AND PLAQUER01HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 1998 to 2006
$1.6M
Aldosterone, G6PD, and Vascular Endothelial FunctionK02HL081110 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LEOPOLD, JANE A · 2005 to 2009
$502k
Selenium, Glutathione Peroxidase-1, and Homocysteine-induced Cardiac RemodelingR21HL089734 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI JOSEPH, JACOB · 2008 to 2009
$413k
STRUCTURAL CHARACTERIZATION OF THE APOPROTEIN E RECEPTORR01HL028178 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI INNERARITY, THOMAS L. · 1986 to 1988
–
NHLBI PROTEOMICS INITIATIVE-N01HV28178N01HV028178 · HV · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COSTELLO, CATHERINE E. · 2002 to 2006
–
NHLBI NIH HHS HL61795NHLBI NIH HHS HL70819NHLBI NIH HHS HL81110NHLBI NIH HHS HL81857NHLBI NIH HHS HV28178NHLBI NIH HHS K02 HL081110NHLBI NIH HHS N01 HV028178NHLBI NIH HHS P01 HL081587NHLBI NIH HHS R01 HL061795NHLBI NIH HHS R01 HL081857NHLBI NIH HHS R21 HL089734NHLBI NIH HHS R37 HL061795NHLBI NIH HHS U54 HL070819
6 · The paper itself

Abstract

In the vasculature, reactive oxidant species, including reactive oxygen, nitrogen, or halogenating species, and thiyl, tyrosyl, or protein radicals may oxidatively modify lipids and proteins with deleterious consequences for vascular function. These biologically active free radical and nonradical species may be produced by increased activation of oxidant-generating sources and/or decreased cellular antioxidant capacity. Once formed, these species may engage in reactions to yield more potent oxidants that promote transition of the homeostatic vascular phenotype to a pathobiological state that is permissive for atherothrombogenesis. This dysfunctional vasculature is characterized by lipid peroxidation and aberrant lipid deposition, inflammation, immune cell activation, platelet activation, thrombus formation, and disturbed hemodynamic flow. Each of these pathobiological states is associated with an increase in the vascular burden of free radical species-derived oxidation products and, thereby, implicates increased oxidant stress in the pathogenesis of atherothrombotic vascular disease.

Indexed as

Oxidative StressCardiovascular DiseasesFree RadicalsHumansLipid PeroxidationOxidoreductasesThrombosisFree RadicalsOxidoreductases

Identifiers

PMID19751821
PMCPMC2797369
OpenAlexW1996370937

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.