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The Biological Bases of Group 2 Pulmonary Hypertension

Department of Cardiology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain
Instituto de Investigación Sanitaria Gregorio Marañón, 28007 Madrid, Spain
Centro de Investigación Biomédica en Red, CIBERCV, Instituto de Salud Carlos III, 28026 Madrid, Spain
Facultad de Medicine, Universidad Complutense de Madrid, 28007 Madrid, Spain
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(23), 5884;
Received: 7 November 2019 / Revised: 20 November 2019 / Accepted: 21 November 2019 / Published: 23 November 2019
(This article belongs to the Special Issue Molecular Research on Pulmonary Hypertension 2.0)
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. View Full-Text
Keywords: pulmonary hypertension group 2; left heart disease; isolated pulmonary hypertension; combined pulmonary hypertension; gene; epigenetics pulmonary hypertension group 2; left heart disease; isolated pulmonary hypertension; combined pulmonary hypertension; gene; epigenetics
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MDPI and ACS Style

Fernández, A.I.; Yotti, R.; González-Mansilla, A.; Mombiela, T.; Gutiérrez-Ibanes, E.; Pérez del Villar, C.; Navas-Tejedor, P.; Chazo, C.; Martínez-Legazpi, P.; Fernández-Avilés, F.; Bermejo, J. The Biological Bases of Group 2 Pulmonary Hypertension. Int. J. Mol. Sci. 2019, 20, 5884.

AMA Style

Fernández AI, Yotti R, González-Mansilla A, Mombiela T, Gutiérrez-Ibanes E, Pérez del Villar C, Navas-Tejedor P, Chazo C, Martínez-Legazpi P, Fernández-Avilés F, Bermejo J. The Biological Bases of Group 2 Pulmonary Hypertension. International Journal of Molecular Sciences. 2019; 20(23):5884.

Chicago/Turabian Style

Fernández, Ana I., 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 Javier Bermejo. 2019. "The Biological Bases of Group 2 Pulmonary Hypertension" International Journal of Molecular Sciences 20, no. 23: 5884.

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