Evidence map›Paper›PMID 24572252›Full record

ArticleJournal of the American Heart Association2014

Mechanism of the susceptibility of remodeled pulmonary vessels to drug-induced cell killing.

Yasmine F Ibrahim, Chi-Ming Wong, Ludmila Pavlickova, Lingling Liu, Lobsang Trasar, Geetanjali Bansal, Yuichiro J Suzuki

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2014. 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
2.7field-weighted citation impact, top 10% 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, 32 citations in OpenAlex.

  1. Article
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  11. Effects of Bcl-2/Bcl-xAntioxidants (Basel, Switzerland) · 2018
    Article
  12. Insights on the epigenetic mechanisms underlying pulmonary arterial hypertension.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018
    Review
  13. Redox Biology of Right-Sided Heart Failure.Antioxidants (Basel, Switzerland) · 2018
    Review
  14. Mitochondrial HSP90 Accumulation Promotes Vascular Remodeling in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

7 authors at 2 institutions in 1 country.

Yasmine F IbrahimDepartment of Pharmacology and Physiology, Georgetown University Medical Center, Washington, 20057, DC.
Chi-Ming Wong
Ludmila Pavlickova
Lingling Liu
Lobsang Trasar
Geetanjali Bansal
Yuichiro J Suzuki
Georgetown University Medical Center · USGeorgetown University · US

Funding

Mechanism of apoptosis in lung vascular smooth muscleR01HL072844 · NHLBI · TUFTS UNIVERSITY BOSTON · PI SUZUKI, YUICHIRO JUSTIN · 2003 to 2017
$3.3M
Oxidant signaling for airway remodeling and inflammationR01HL097514 · NHLBI · GEORGETOWN UNIVERSITY · PI SUZUKI, YUICHIRO JUSTIN · 2009 to 2012
$1.4M
NHLBI NIH HHS R01 HL072844NHLBI NIH HHS R01 HL097514NHLBI NIH HHS R01HL72844NHLBI NIH HHS R01HL97514
6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension remains a devastating disease without a cure. The major complication of this disease is the abnormal growth of vascular cells, resulting in pulmonary vascular remodeling. Thus, agents, which affect the remodeled vessels by killing unwanted cells, should improve treatment strategies. The present study reports that antitumor drugs selectively kill vascular cells in remodeled pulmonary vessels in rat models of pulmonary hypertension. METHODS AND

resultsAfter developing pulmonary vascular remodeling in chronic hypoxia or chronic hypoxia/SU-5416 models, rats were injected with antitumor drugs including proteasome inhibitors (bortezomib and MG-132) and daunorubicin. Within 1 to 3 days, these agents reduced the media and intima thickness of remodeled pulmonary vascular walls, but not the thickness of normal pulmonary vessels. These drugs also promoted apoptotic and autophagic death of vascular cells in the remodeled vessels, but not in normal vessels. We provide evidence that the upregulation of annexin A1, leading to GATA4-dependent downregulation of Bcl-xL, is a mechanism for specific apoptotic killing, and for the role of parkin in defining specificity of autophagic killing of remodeled vascular cells. The reversal of pulmonary vascular remodeling increased the capacity of vasodilators to reduce pulmonary arterial pressure.

conclusionsThese results suggest that antitumor drugs can specifically kill cells in remodeled pulmonary vascular walls and may be useful for improving the efficacy of current therapeutic strategies to treat pulmonary arterial hypertension.

Indexed as

AnimalsAnnexin A1Antineoplastic AgentsApoptosisArterial PressureAutophagybcl-X ProteinCells, CulturedDisease Models, AnimalFamilial Primary Pulmonary HypertensionGATA4 Transcription FactorHeart VentriclesHumansHypertension, PulmonaryHypoxiaMaleAnnexin A1Antineoplastic AgentsBcl2l1 protein, ratbcl-X ProteinGata4 protein, ratGATA4 Transcription Factorparkin proteinUbiquitin-Protein LigasesVasodilator Agentsapoptosisautophagyblood pressurepulmonary hypertensionvascular remodeling

Identifiers

PMID24572252
PMCPMC3959719
OpenAlexW2137981028

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.