Evidence map›Paper›PMID 20060403›Full record

ReviewSteroids2010

Estrogen and oxidative stress: A novel mechanism that may increase the risk for cardiovascular disease in women.

Richard E White, Ross Gerrity, Scott A Barman, Guichun Han

Open access · greenAbstract readReview
In one paragraph

Review in Steroids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. An In Vivo Model of Estrogen Supplementation Concerning the Expression of CaJournal of cardiovascular development and disease · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Observational
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Richard E WhiteDepartment of Pharmacology & Toxicology, Medical College of Georgia, Augusta, GA 30912, United States. rwhite@mcg.edu
Ross Gerrity
Scott A Barman
Guichun Han
Augusta University · USTexas A&M University · US

Funding

PKC Signaling in cAMP-Induced Pulmonary VasodilationR01HL068026 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BARMAN, SCOTT A · 2001 to 2010
$2.3M
Estrogen dual effects on coronary arteriesR01HL073890 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WHITE, RICHARD E · 2005 to 2008
$1.3M
MOLECULAR BASIS OF CAMP INDUCED CORONARY VASORELAXATIONR01HL064779 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI WHITE, RICHARD E · 2000 to 2003
$901k
MINORITY HYPERTENSION RESEARCH DEVELOPMENT TRAININGT35HL007389 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CARDOSO, SERGIO S · 1985 to 1987
–
NHLBI NIH HHS HL07389NHLBI NIH HHS HL-64779NHLBI NIH HHS HL-68026NHLBI NIH HHS R01 HL064779NHLBI NIH HHS R01 HL068026NHLBI NIH HHS R01 HL073890
6 · The paper itself

Abstract

Although early studies demonstrated that exogenous estrogen lowered a woman's risk of cardiovascular disease, recent trials indicate that HRT actually increases the risk of coronary heart disease or stroke. However, there is no clear explanation for this discrepancy. Is estrogen a helpful or a harmful hormone in terms of cardiovascular function? This review discusses some recent findings that propose a novel mechanism which may shed significant light upon this controversy. We propose that nitric oxide synthase (NOS) expressed within the vascular wall is a target of estrogen action. Under normal conditions in younger women, the primary product of estrogen action is NO, which produces a number of beneficial effects on vascular biology. As a woman ages, however, there is evidence for loss of important molecules essential for NO production (e.g., tetrahydrobiopterin, l-arginine). As these molecules are depleted, NOS becomes increasingly "uncoupled" from NO production, and instead produces superoxide, a dangerous reactive oxygen species. We propose that a similar uncoupling and reversal of estrogen response occurs in diabetes. Therefore, we propose that estrogen is neither "good" nor "bad", but simply stimulates NOS activity. It is the biochemical environment around NOS that will determine whether estrogen produces a beneficial (NO) or deleterious (superoxide) product, and can account for this dual and opposite nature of estrogen pharmacology. Further, this molecular mechanism is consistent with recent analyses revealing that HRT produces salutary effects in younger women, but mainly increases the risk of cardiovascular dysfunction in older postmenopausal women.

Indexed as

Oxidative StressCardiovascular DiseasesEstrogen Replacement TherapyEstrogensFemaleHumansMuscle, Smooth, VascularNitric OxideNitric Oxide SynthaseSuperoxidesEstrogensNitric OxideNitric Oxide SynthaseSuperoxides

Identifiers

PMID20060403
PMCPMC2891201
OpenAlexW2052572660

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.