Evidence map›Paper›PMID 19577709›Full record

ArticleTrends in cardiovascular medicine2009

Cyclooxygenase-2 inhibition and hypoxia-induced pulmonary hypertension: effects on pulmonary vascular remodeling and contractility.

Laura E Fredenburgh, Jun Ma, Mark A Perrella

Open access · greenAbstract read
In one paragraph

Article in Trends in cardiovascular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

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  5. The effect of patent ductus arteriosus treatment with paracetamol on pulmonary vascular resistance.Journal of perinatology : official journal of the California Perinatal Association · 2022
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  14. Effects ofEvidence-based complementary and alternative medicine : eCAM · 2018
    Article
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  17. Expression profile of mitochondrial voltage-dependent anion channel-1 (VDAC1) influenced genes is associated with pulmonary hypertension.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017
    Article
  18. Article
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  20. Genetically manipulated mouse models of lung disease: potential and pitfalls.American journal of physiology. Lung cellular and molecular physiology · 2012
    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

3 authors at 1 institution in 1 country.

Laura E FredenburghDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. lfredenburgh@rics.bwh.harvard.edu.
Jun Ma
Mark A Perrella
Brigham and Women's Hospital · US

Funding

RESPIRATORY RESEARCHT32HL007633 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI George R Washko · 1985 to 2026
$14.9M
Role of Heme Oxygenase-1 in SepsisR01HL060788 · NHLBI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI PERRELLA, MARK A · 1998 to 2010
$4.1M
REGULATION OF NITRIC OXIDE GENE EXPRESSION IN SEPSISR01GM053249 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI PERRELLA, MARK A · 1995 to 2008
$2.0M
Role of Cyclooxygenase-2-derived Prostanoids in Polymicrobial SepsisK08GM083207 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI FREDENBURGH, LAURA ELIZABETH · 2008 to 2012
$752k
NHLBI NIH HHS HL0007633NHLBI NIH HHS R01 HL060788NHLBI NIH HHS R01 HL60788NHLBI NIH HHS T32 HL007633NIGMS NIH HHS K08 GM083207NIGMS NIH HHS R01 GM053249
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a significant disease process characterized by elevated pulmonary vascular resistance leading to increased right ventricular afterload and ultimately progressing to right ventricular dysfunction and often death. Irreversible remodeling of the pulmonary vasculature is the hallmark of pulmonary hypertension and frequently leads to progressive functional decline in patients with PAH despite treatment with currently available therapies. Metabolites of the arachidonic acid cascade play an important homeostatic role in the pulmonary vasculature, and dysregulation of pathways downstream of arachidonic acid plays a central role in the pathobiology of PAH. Cyclooxygenase-2 (COX-2) is up-regulated in pulmonary artery smooth muscle cells (PASMC) and inflammatory cells during hypoxia and plays a protective role in the lung's response to hypoxia. We recently demonstrated that absence of COX-2 was detrimental in a mouse model of hypoxia-induced pulmonary hypertension. Exposure of COX-2 null mice to hypoxia resulted in severe pulmonary hypertension characterized by enhanced pulmonary vascular remodeling and significant up-regulation of the endothelin-1 receptor ET(A)R in the lung after hypoxia. Absence of COX-2 in vitro led to enhanced contractility of PASMC after exposure to hypoxia, which could be attenuated by iloprost, a prostaglandin I(2) analog. These findings suggest that selective inhibition of COX-2 may have detrimental pulmonary vascular consequences in patients with preexisting pulmonary hypertension or underlying hypoxemic lung diseases. Here, we discuss our recent data demonstrating the adverse consequences of COX-2 inhibition on pulmonary vascular remodeling and PASMC contractility.

Indexed as

AnimalsArachidonic AcidCell ProliferationCyclooxygenase 2Cyclooxygenase 2 InhibitorsDisease Models, AnimalHumansHypertension, PulmonaryHypoxiaIloprostMiceMice, KnockoutMuscle, Smooth, VascularPulmonary ArterySignal TransductionVasoconstrictionArachidonic AcidCyclooxygenase 2Cyclooxygenase 2 InhibitorsIloprostPtgs2 protein, mouseVasodilator Agents

Identifiers

PMID19577709
PMCPMC2746907
OpenAlexW1996985763

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.