Evidence map›Paper›PMID 29047100›Full record

ReviewAdvances in experimental medicine and biology2017

Mitochondrial and Metabolic Drivers of Pulmonary Vascular Endothelial Dysfunction in Pulmonary Hypertension.

Qiujun Yu, Stephen Y Chan

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
27.3field-weighted citation impact, top 1% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

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  15. Cystathionine beta synthase regulates mitochondrial dynamics and function in endothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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 2 institutions in 1 country.

Qiujun YuCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh Medical Center, 200 Lothrop Street BST1704.2, Pittsburgh, PA, 15261, USA.
Stephen Y ChanCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh Medical Center, 200 Lothrop Street BST1704.2, Pittsburgh, PA, 15261, USA. chansy@pitt.edu.
University of Pittsburgh · USUniversity of Pittsburgh Medical Center · 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
Functions of the Hypoxia-Induced MicroRNA-210 in Pulmonary Vascular EndotheliumK08HL096834 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CHAN, STEPHEN Y · 2010 to 2014
$687k
NHLBI NIH HHS K08 HL096834NHLBI NIH HHS R01 HL122596NHLBI NIH HHS R01 HL124021
6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a deadly and increasingly prevalent vascular disease characterized by excessive pulmonary vascular remodeling and right ventricular dysfunction which leads to right heart failure, multiorgan dysfunction, and premature death. The cause of the vascular remodeling in PH remains elusive, and thus current treatments are marginally effective and prognosis of PH remains poor. Increasing evidence indicates the pathogenic importance of endothelial dysfunction in PH. However, the underlying mechanisms of such dysfunction are not well described. Endothelial apoptosis and hyperproliferation have been identified in patients with PH. Both are linked with the increased oxidative stress and inflammatory responses, and are influenced by various genetic and exogenous stresses. Importantly, contrary to historic dogma that suggested a negligible role for mitochondria and energy balance in endothelial pathology, recent findings have implicated the role of endothelial metabolism directly in PH. This chapter addresses the emerging role of mitochondria in pulmonary vascular endothelial dysfunction in PH. A more sophisticated understanding of the biochemical, metabolic, molecular, and physiologic underpinnings of this emerging paradigm should enable the development of a new generation of targeted therapies that will stunt or reverse pulmonary vascular remodeling.

Indexed as

Energy MetabolismAnimalsApoptosisEndothelial CellsEndothelium, VascularHumansHypertension, PulmonaryMitochondriaPulmonary ArteryVascular RemodelingEndothelial cellMetabolismMitochondriaPulmonary hypertension

Identifiers

PMID29047100
PMCPMC5810356
OpenAlexW2766674089

What OpenQuestion holds

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LicenceTDM
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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.