Evidence map›Paper›PMID 24039255›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013

Pulmonary veins in the normal lung and pulmonary hypertension due to left heart disease.

James M Hunt, Brian Bethea, Xiang Liu, Aneta Gandjeva, Pradeep P A Mammen, Elvira Stacher, Marina R Gandjeva, Elisabeth Parish, Mario Perez, Lynelle Smith and 3 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

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  8. Clinical-imaging-pathological correlation in pulmonary hypertension associated with left heart disease.European respiratory review : an official journal of the European Respiratory Society · 2024
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  14. Animal models of pulmonary hypertension due to left heart disease.Animal models and experimental medicine · 2022
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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

13 authors at 5 institutions in 5 countries.

James M HuntProgram in Translational Lung Research, Division of Pulmonary Sciences and Critical Care Medicine, Univ. of Colorado Denver, Anschutz Medical Campus, Research 2 - 9th floor, Rm. 9001; Mail stop C-272, 12700 East 19th Ave., Aurora, CO 80045. rubin.tuder@ucdenver.edu.
Brian Bethea
Xiang Liu
Aneta Gandjeva
Pradeep P A Mammen
Elvira Stacher
Marina R Gandjeva
Elisabeth Parish
Mario Perez
Lynelle Smith
Brian B Graham
Wolfgang M Kuebler
Rubin M Tuder
University of Colorado Anschutz Medical Campus · USThe University of Texas Southwestern Medical Center · USCharité - Universitätsmedizin Berlin · DELudwig Boltzmann Institute for Lung Vascular Research · ATSt. Michael's Hospital · CA

Funding

Cytoglobin: A stress-responsive hemoprotein modulating cardiomyocyte survivalR01HL102478 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MAMMEN, PRADEEP P.A. · 2012 to 2016
$2.0M
Zipcode based nano-imaging of hypertensive pulmonary arteriesRC1HL100849 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M. · 2009 to 2010
$1000k
Schistosomiasis Associated Pulmonary Arterial HypertensionK08HL105536 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI GRAHAM, BRIAN BARKLEY · 2011 to 2015
$653k
NHLBI NIH HHS HL 102478NHLBI NIH HHS K08 HL105536NHLBI NIH HHS KO8 HL 105536NHLBI NIH HHS R01 HL102478NHLBI NIH HHS RC1 HL 100849
6 · The paper itself

Abstract

Despite the importance of pulmonary veins in normal lung physiology and the pathobiology of pulmonary hypertension with left heart disease (PH-LHD), pulmonary veins remain largely understudied. Difficult to identify histologically, lung venous endothelium or smooth muscle cells display no unique characteristic functional and structural markers that distinguish them from pulmonary arteries. To address these challenges, we undertook a search for unique molecular markers in pulmonary veins. In addition, we addressed the expression pattern of a candidate molecular marker and analyzed the structural pattern of vascular remodeling of pulmonary veins in a rodent model of PH-LHD and in lung tissue of patients with PH-LHD obtained at time of placement on a left ventricular assist device. We detected urokinase plasminogen activator receptor (uPAR) expression preferentially in normal pulmonary veins of mice, rats, and human lungs. Expression of uPAR remained elevated in pulmonary veins of rats with PH-LHD; however, we also detected induction of uPAR expression in remodeled pulmonary arteries. These findings were validated in lungs of patients with PH-LHD. In selected patients with sequential lung biopsy at the time of removal of the left ventricular assist device, we present early data suggesting improvement in pulmonary hemodynamics and venous remodeling, indicating potential regression of venous remodeling in response to assist device treatment. Our data indicate that remodeling of pulmonary veins is an integral part of PH-LHD and that pulmonary veins share some key features present in remodeled yet not normotensive pulmonary arteries.

Indexed as

AdolescentAdultAgedAnimalsBlotting, WesternCase-Control StudiesCell ProliferationChildEndothelium, VascularFemaleFluorescent Antibody TechniqueHeart-Assist DevicesHeart DiseasesHemodynamicsHumansHypertension, PulmonaryReceptors, Urokinase Plasminogen ActivatorRNA, Messengerleft heart failurepulmonary circulationpulmonary hypertensionpulmonary veinsvessel remodeling

Identifiers

PMID24039255
PMCPMC3840271
OpenAlexW2148739223

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.