Evidence map›Paper›PMID 25827602›Full record

ReviewEuropean heart journal2015

Haeme oxygenase signalling pathway: implications for cardiovascular disease.

Laura E Fredenburgh, Allison A Merz, Susan Cheng

Abstract readReview
In one paragraph

Review in European heart journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
–field-weighted citation impact
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

35 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Do patients benefit from omega-3 fatty acids?Cardiovascular research · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Antithrombotic effects of heme-degrading and heme-binding proteins.American journal of physiology. Heart and circulatory physiology · 2020
    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.

Laura E FredenburghDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA lfredenburgh@rics.bwh.harvard.edu scheng@rics.bwh.harvard.edu.
Allison A MerzDivision of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Susan ChengDivision of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Framingham Heart Study, Framingham, MA, USA lfredenburgh@rics.bwh.harvard.edu scheng@rics.bwh.harvard.edu.

Funding

Mesenchymal Stromal Cell Conditioning by Carbon MonoxideP01HL108801 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHOI, AUGUSTINE M · 2011 to 2015
$13.8M
Mechanobiology of Vascular Remodeling in Pulmonary Arterial HypertensionR01HL114839 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FREDENBURGH, LAURA ELIZABETH · 2012 to 2016
$2.1M
Myocardial and Arterial Aging: Spectrum, Correlates, and PrognosisR00HL107642 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHENG, SUSAN · 2014 to 2016
$747k
Arterial Stiffness in the Pathogenesis of Human Pulmonary Arterial HypertensionR03HL115106 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FREDENBURGH, LAURA ELIZABETH · 2012 to 2013
$174k
NHLBI NIH HHS P01 HL108801NHLBI NIH HHS P01HL108801NHLBI NIH HHS R00HL107642NHLBI NIH HHS R01HL114839NHLBI NIH HHS R03HL115106
6 · The paper itself

Abstract

Evidence now points to the haeme oxygenase (HO) pathway as a possible actor in modulating risk for cardiovascular disease (CVD). In particular, the HO pathway may represent a key endogenous modulator of oxidative, inflammatory, and cytotoxic stress while also exhibiting vasoregulatory properties. In this review, we summarize the accumulating experimental and emerging clinical data indicating how activity of the HO pathway and its products may play a role in mechanisms underlying the development of CVD. We also identify gaps in the literature to date and suggest future directions for investigation. Because HO pathway activity can be influenced not only by genetic traits and environmental stimuli but also by a variety of existing pharmacologic interventions, the pathway could serve as a prime target for reducing the overall burden of CVD. Further work is needed to determine the role of HO pathway products as possible prognostic markers of risk for clinical CVD events and the extent to which therapeutic augmentation or inhibition of HO pathway activity could serve to modify CVD risk.

Indexed as

AntioxidantsApoptosisCardiovascular DiseasesCell ProliferationForecastingGene ExpressionHemeHeme Oxygenase (Decyclizing)HumansInflammation MediatorsPlatelet AggregationRisk FactorsSignal TransductionThrombosisVasoconstrictionVasodilationAntioxidantsHemeHeme Oxygenase (Decyclizing)Inflammation MediatorsBilirubinBiliverdinCarbon monoxideCardiovascular diseaseHeme oxygenase pathway

Identifiers

PMID25827602
PMCPMC4475572

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.