Evidence map›Paper›PMID 23334338›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2013

Vascular remodeling in pulmonary hypertension.

Larissa A Shimoda, Steven S Laurie

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
12.1field-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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 228 citations in OpenAlex.

  1. A Cross-Species and Sex-Specific Meta-Analysis of Transcriptomic Studies of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2025
    Pooled it
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68 more citing papers are in PubMed but not listed here.

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.

Larissa A ShimodaDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, MD 21224, USA. shimodal@welch.jhu.edu
Steven S Laurie
Johns Hopkins University · US

Funding

MULTIDISCIPLINARY TRAINING PROGRAM IN LUNG DISEASEST32HL007534 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI Nadia N Hansel, Larissa A. Shimoda · 1985 to 2026
$28.3M
Na+/H+ exchange in pulmonary hypertensionR01HL073859 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2003 to 2020
$4.2M
Chronic hypoxia and pulmonary vascular smooth muscleR01HL067191 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2003 to 2010
$1.9M
Clinical System for Arterial CharacterizationR44HL073589 · NHLBI · NEWTON LABORATORIES · PI FULGHUM, STEPHEN FREDERICK · 2005 to 2006
$743k
Interrogation of the Cellular Pathogenesis of Pulmonary HypertensionR21HL096982 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2011 to 2012
$451k
Functional linkage of NHE1 and calpain in IPAHR03HL114902 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SHIMODA, LARISSA A. · 2012 to 2013
$158k
Clinical System for Arterial Tissue CharacterizationR43HL073589 · NHLBI · NEWTON LABORATORIES · PI FULGHUM, STEPHEN FREDERICK · 2004 to 2004
$100k
NHLBI NIH HHS HL073589NHLBI NIH HHS HL096982NHLBI NIH HHS HL114902NHLBI NIH HHS HL67191NHLBI NIH HHS R01 HL067191NHLBI NIH HHS R01 HL073859NHLBI NIH HHS R03 HL114902NHLBI NIH HHS R21 HL096982NHLBI NIH HHS R43 HL073589NHLBI NIH HHS R44 HL073589NHLBI NIH HHS T32 HL007534
6 · The paper itself

Abstract

Pulmonary hypertension is a complex, progressive condition arising from a variety of genetic and pathogenic causes. Patients present with a spectrum of histologic and pathophysiological features, likely reflecting the diversity in underlying pathogenesis. It is widely recognized that structural alterations in the vascular wall contribute to all forms of pulmonary hypertension. Features characteristic of the remodeled vasculature in patients with pulmonary hypertension include increased stiffening of the elastic proximal pulmonary arteries, thickening of the intimal and/or medial layer of muscular arteries, development of vaso-occlusive lesions, and the appearance of cells expressing smooth muscle-specific markers in normally non-muscular small diameter vessels, resulting from proliferation and migration of pulmonary arterial smooth muscle cells and cellular transdifferentiation. The development of several animal models of pulmonary hypertension has provided the means to explore the mechanistic underpinnings of pulmonary vascular remodeling, although none of the experimental models currently used entirely replicates the pulmonary arterial hypertension observed in patients. Herein, we provide an overview of the histological abnormalities observed in humans with pulmonary hypertension and in preclinical models and discuss insights gained regarding several key signaling pathways contributing to the remodeling process. In particular, we will focus on the roles of ion homeostasis, endothelin-1, serotonin, bone morphogenetic proteins, Rho kinase, and hypoxia-inducible factor 1 in pulmonary arterial smooth muscle and endothelial cells, highlighting areas of cross-talk between these pathways and potentials for therapeutic targeting.

Indexed as

AnimalsBone Morphogenetic ProteinsDisease Models, AnimalEndothelin-1Familial Primary Pulmonary HypertensionHumansHypertension, PulmonaryHypoxia-Inducible Factor 1MicePulmonary ArteryRatsrho-Associated KinasesSerotoninSignal TransductionBone Morphogenetic ProteinsEndothelin-1Hypoxia-Inducible Factor 1rho-Associated KinasesSerotonin

Identifiers

PMID23334338
PMCPMC3584237
OpenAlexW1979129486

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.