Evidence map›Paper›PMID 30926336›Full record

ReviewThe American journal of pathology2019

Plexiform Arteriopathy in Rodent Models of Pulmonary Arterial Hypertension.

Brandon L Carman, Dan N Predescu, Roberto Machado, Sanda A Predescu

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  13. Xbp1s-Ddit3 promotes MCT-induced pulmonary hypertension.Clinical science (London, England : 1979) · 2021
    Article
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  20. 3DFrontiers in bioengineering and biotechnology · 2020
    Article
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

4 authors at 2 institutions in 1 country.

Brandon L CarmanDivision of Pulmonary Critical Care and Sleep Medicine, Department of Internal Medicine, Rush Medical College, Chicago, Illinois.
Dan N PredescuDivision of Pulmonary Critical Care and Sleep Medicine, Department of Internal Medicine, Rush Medical College, Chicago, Illinois.
Roberto MachadoDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, Indiana.
Sanda A PredescuDivision of Pulmonary Critical Care and Sleep Medicine, Department of Internal Medicine, Rush Medical College, Chicago, Illinois. Electronic address: sanda_predescu@rush.edu.
Rush University Medical Center · USIndiana University – Purdue University Indianapolis · US

Funding

Cleavage of Intersectin-1s by Granzyme B and Pulmonary Arterial HypertensionR01HL127022 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI PREDESCU, SANDA A · 2015 to 2024
$3.1M
NHLBI NIH HHS R01 HL127022
6 · The paper itself

Abstract

As time progresses, our understanding of disease pathology is propelled forward by technological advancements. Much of the advancements that aid in understanding disease mechanics are based on animal studies. Unfortunately, animal models often fail to recapitulate the entirety of the human disease. This is especially true with animal models used to study pulmonary arterial hypertension (PAH), a disease with two distinct phases. The first phase is defined by nonspecific medial and adventitial thickening of the pulmonary artery and is commonly reproduced in animal models, including the classic models (ie, hypoxia-induced pulmonary hypertension and monocrotaline lung injury model). However, many animal models, including the classic models, fail to capture the progressive, or second, phase of PAH. This is a stage defined by plexogenic arteriopathy, resulting in obliteration and occlusion of the small- to mid-sized pulmonary vessels. Each of these two phases results in severe pulmonary hypertension that directly leads to right ventricular hypertrophy, decompensated right-sided heart failure, and death. Fortunately, newly developed animal models have begun to address the second, more severe, side of PAH and aid in our ability to develop new therapeutics. Moreover, p38 mitogen-activated protein kinase activation emerges as a central molecular mediator of plexiform lesions in both experimental models and human disease. Therefore, this review will focus on plexiform arteriopathy in experimental animal models of PAH.

Indexed as

Disease Models, AnimalAnimalsDisease ProgressionHumansHypoxiaIndolesMAP Kinase Signaling SystemMiceMice, KnockoutPulmonary Arterial HypertensionPulmonary ArteryPyrrolesRatsIndolesPyrrolesSemaxinib

Identifiers

PMID30926336
PMCPMC6584781
OpenAlexW2923924591

What Socratic 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 Socratic graph.