Evidence map›Paper›PMID 31771195›Full record

ReviewInternational journal of molecular sciences2019

The Biological Bases of Group 2 Pulmonary Hypertension.

Ana I Fernández, Raquel Yotti, Ana González-Mansilla, Teresa Mombiela, Enrique Gutiérrez-Ibanes, Candelas Pérez Del Villar, Paula Navas-Tejedor, Christian Chazo, Pablo Martínez-Legazpi, Francisco Fernández-Avilés and 1 more

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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  12. Pulmonary Hypertension in Heart Failure.International journal of heart failure · 2021
    Review
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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

11 authors.

Ana I FernándezDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Raquel YottiDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Ana González-MansillaDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.ORCID 0000-0003-3578-9606
Teresa MombielaDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Enrique Gutiérrez-IbanesDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Candelas Pérez Del VillarDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Paula Navas-TejedorDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Christian ChazoDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Pablo Martínez-LegazpiDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Francisco Fernández-AvilésDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Javier BermejoDepartment of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a potentially fatal condition with a prevalence of around 1% in the world population and most commonly caused by left heart disease (PH-LHD). Usually, in PH-LHD, the increase of pulmonary pressure is only conditioned by the retrograde transmission of the left atrial pressure. However, in some cases, the long-term retrograde pressure overload may trigger complex and irreversible biomechanical and biological changes in the pulmonary vasculature. This latter clinical entity, designated as combined pre- and post-capillary PH, is associated with very poor outcomes. The underlying mechanisms of this progression are poorly understood, and most of the current knowledge comes from the field of Group 1-PAH. Treatment is also an unsolved issue in patients with PH-LHD. Targeting the molecular pathways that regulate pulmonary hemodynamics and vascular remodeling has provided excellent results in other forms of PH but has a neutral or detrimental result in patients with PH-LHD. Therefore, a deep and comprehensive biological characterization of PH-LHD is essential to improve the diagnostic and prognostic evaluation of patients and, eventually, identify new therapeutic targets. Ongoing research is aimed at identify candidate genes, variants, non-coding RNAs, and other biomarkers with potential diagnostic and therapeutic implications. In this review, we discuss the state-of-the-art cellular, molecular, genetic, and epigenetic mechanisms potentially involved in PH-LHD. Signaling and effective pathways are particularly emphasized, as well as the current knowledge on -omic biomarkers. Our final aim is to provide readers with the biological foundations on which to ground both clinical and pre-clinical research in the field of PH-LHD.

Indexed as

AnimalsEpigenomicsHeart FailureHemodynamicsHumansHypertension, PulmonaryReactive Oxygen SpeciesVentricular Dysfunction, LeftReactive Oxygen Speciescombined pulmonary hypertensionepigeneticsgeneisolated pulmonary hypertensionleft heart diseasepulmonary hypertension group 2

Identifiers

PMID31771195
PMCPMC6928720

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Registered trials

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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.