Evidence map›Paper›PMID 30773044›Full record

ReviewJournal of cardiovascular pharmacology and therapeutics2019

The Search for Disease-Modifying Therapies in Pulmonary Hypertension.

Chen-Shan Chen Woodcock, Stephen Y Chan

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology and therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
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  13. Matrix stiffening induces a pathogenic QKI-miR-7-SRSF1 signaling axis in pulmonary arterial endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2021
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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

2 authors at 1 institution in 1 country.

Chen-Shan Chen Woodcock1 Division of Cardiology, Department of Medicine, Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Stephen Y Chan1 Division of Cardiology, Department of Medicine, Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.ORCID 0000-0002-9520-7527
University of Pittsburgh · US

Funding

Defining the Complex Biology of the miR-130/301 Family in Pulmonary HypertensionR01HL124021 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2014 to 2025
$4.9M
Iron-Sulfur Deficiency as a Critical Pathogenic Cause of Pulmonary HypertensionR01HL122596 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2015 to 2024
$4.5M
Molecular Drivers of Vascular Stiffness and Metabolic Dysfunction in HIV-Induced Pulmonary Arterial HypertensionR01HL138437 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y, NORRIS, KAREN A · 2017 to 2020
$2.4M
RNA editing controls pulmonary endothelial pathophenotypes in pulmonary hypertensionR00HL161320 · NHLBI · NATIONAL JEWISH HEALTH · PI Chen-Shan Julia Woodcock · 2024 to 2026
$747k
Computational repurposing of chemotherapies for pulmonary hypertensionUH2TR002073 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2017 to 2018
$615k
RNA editing controls pulmonary endothelial pathophenotypes in pulmonary hypertensionK99HL161320 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WOODCOCK, CHEN-SHAN JULIA · 2022 to 2023
$212k
Computational repurposing of chemotherapies for pulmonary hypertensionUH3TR002073 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2019 to 2019
$155k
NCATS NIH HHS UH2 TR002073NCATS NIH HHS UH3 TR002073NHLBI NIH HHS K99 HL161320NHLBI NIH HHS R00 HL161320NHLBI NIH HHS R01 HL122596NHLBI NIH HHS R01 HL124021NHLBI NIH HHS R01 HL138437
6 · The paper itself

Abstract

Pulmonary hypertension (PH) and its severe subtype pulmonary arterial hypertension (PAH) encompass a set of multifactorial diseases defined by sustained elevation of pulmonary arterial pressure and pulmonary vascular resistance leading to right ventricular failure and subsequent death. Pulmonary hypertension is characterized by vascular remodeling in association with smooth muscle cell proliferation of the arterioles, medial thickening, and plexiform lesion formation. Despite our recent advances in understanding its pathogenesis and related therapeutic discoveries, PH still remains a progressive disease without a cure. Nevertheless, development of drugs that specifically target molecular pathways involved in disease pathogenesis has led to improvement in life quality and clinical outcomes in patients with PAH. There are presently more than 12 Food and Drug Administration-approved vasodilator drugs in the United States for the treatment of PAH; however, mortality with contemporary therapies remains high. More recently, there have been exuberant efforts to develop new pharmacologic therapies that target the fundamental origins of PH and thus could represent disease-modifying opportunities. This review aims to summarize recent developments on key signaling pathways and molecular targets that drive PH disease progression, with emphasis on new therapeutic options under development.

Indexed as

AnimalsAntihypertensive AgentsArterial PressureHumansMolecular Targeted TherapyPulmonary Arterial HypertensionPulmonary ArterySignal TransductionTreatment OutcomeVascular RemodelingVasodilator AgentsAntihypertensive AgentsVasodilator AgentsDNA damageepigeneticsinflammationmetabolismmolecular pathologyproliferationpulmonary artery hypertensionvascular function

Identifiers

PMID30773044
PMCPMC6714051
OpenAlexW2917570538

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.