Targeting Vascular Remodeling to Treat Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) describes a group of conditions with a common hemodynamic phenotype of increased pulmonary artery pressure, driven by progressive remodeling of small pulmonary arteries, leading to right heart failure and death. Vascular remodeling is the key pathological featur...

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Bibliographic Details
Published in:Trends in molecular medicine 2017-01, Vol.23 (1), p.31-45
Main Authors: Thompson, A.A. Roger, Lawrie, Allan
Format: Article
Language:English
Subjects:
Animals
Arteries
BMPR2
Bone Morphogenetic Protein Receptors, Type II - genetics
Bone Morphogenetic Protein Receptors, Type II - metabolism
Deoxyribonucleic acid
DNA
DNA damage
Drug Discovery
Epigenetics
Heart diseases
Heart failure
Humans
Hypertension
Hypertension, Pulmonary - drug therapy
Hypertension, Pulmonary - genetics
Hypertension, Pulmonary - metabolism
Hypertension, Pulmonary - physiopathology
hypoxia
Hypoxia - drug therapy
Hypoxia - genetics
Hypoxia - metabolism
Hypoxia - physiopathology
Metabolism
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Molecular Targeted Therapy
Pathogenesis
Pathology
Pulmonary arteries
Pulmonary artery
Pulmonary Artery - drug effects
Pulmonary Artery - metabolism
Pulmonary Artery - pathology
Pulmonary hypertension
Signal Transduction - drug effects
vascular remodeling
Vascular Remodeling - drug effects
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Description
Summary:Pulmonary arterial hypertension (PAH) describes a group of conditions with a common hemodynamic phenotype of increased pulmonary artery pressure, driven by progressive remodeling of small pulmonary arteries, leading to right heart failure and death. Vascular remodeling is the key pathological feature of PAH, but treatments targeting this process are lacking. In this review, we summarize important advances in our understanding of PAH pathogenesis from novel genetic and epigenetic factors, to cell metabolism and DNA damage. We show how these processes may integrate and highlight exploitable targets that could alter the relentless vascular remodeling in PAH.
ISSN:1471-4914
1471-499X
DOI:10.1016/j.molmed.2016.11.005