High-Frequency Oscillatory Ventilation, MicroRNAs in Pulmonary Hypertension, and Gastric Residual Volumes

Ortiz, Maria Gabriela Tupayachi; Krick, Stefanie; Cano, J.

doi:10.1164/rccm.201304-0672rr

Cited by 1 publication

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“…MiRNA are believed to coordinate and regulate multiple disease pathways in the pulmonary vasculature. More than 100 studies have reported associations between more than 30 miRNAs and different non-Group 2 forms of PH [127,128,129,130,131]. Amongst them, the most promising results have been identified in PAH: miR-21 [132], miR-17/92 [133], miR-204 [134], miR-130/301 [131], and Let-7d-3p [135].…”

Section: The Epigenetics Of Ph-lhdmentioning

confidence: 99%

The Biological Bases of Group 2 Pulmonary Hypertension

Fernández

Yotti

González‐Mansilla

et al. 2019

IJMS

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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.

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