The Shared Pathogenesis of Pulmonary Artery Hypertension

https://doi.org/10.22146/aci.36635

Anggoro Budi Hartopo(1*), Lucia Kris Dinarti(2)

(1) Department of Cardiology and Vascular Medicine, Faculty of Medicine, Public Heath and Nursing, Universitas Gadjah Mada - Dr. Sardjito Hospital Yogyakarta, Indonesia
(2) Department of Cardiology and Vascular Medicine, Faculty of Medicine, Public Heath and Nursing, Universitas Gadjah Mada - Dr. Sardjito Hospital Yogyakarta, Indonesia
(*) Corresponding Author

Abstract


Pulmonary artery hypertension is defined as an increased in pulmonary artery pressure
exceeding 25 mmHg with normal pulmonary wedge pressure. The pathogenesis of pulmonary
artery hypertension involves interaction among vascular, cellular and biomarker components
in the pulmonary tissue; with eventual result is elevated pulmonary artery pressure. Vascular
components are remodeling of intimal, medial and adventitial layers. Cellular components are
played by apoptosis-resistant endothelial cells, proliferative-prone pulmonary artery smooth
muscle cells, fibroblasts and inflammatory cells. The functional biomarkers are produced and
mediated by these cellular changes, mainly endothelin-1, thromboxane, serotonin, nitric oxide,
and prostacyclin. The pulmonary vascular remodeling in pulmonary artery hypertension are
diverse and may present in various severity based on underlying etiology. Understanding the
shared pathogenesis in pulmonary artery hypertension is of paramount importance in order to
improve the disease management and treatment approach.


Keywords


pulmonary artery hypertension; pathogenesis; pulmonary vascular remodeling

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DOI: https://doi.org/10.22146/aci.36635

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Copyright (c) 2018 Anggoro Budi Hartopo, Lucia Kris Dinarti

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