Pulmonary Arterial Hypertension: From Molecular Mechanisms to Novel Therapeutic Approaches

Dear Colleagues,

Pulmonary hypertension (PH) comprises a group of severe clinical disorders, including pulmonary arterial hypertension (PAH), classified according to the World Health Organization (WHO) as Group 1 of PH. PAH is a chronic, progressive, and incurable disease of multifactorial pathobiology. PAH is characterized by vasoconstriction of the pulmonary vessels, an increase in pulmonary vascular resistance, and vascular tone. The remodeling in PAH is associated with endothelial cell dysfunction and intimal thickening, enhanced proliferation and a reduction in apoptosis of pulmonary smooth muscle cells, loss of pre-capillary arteries, perivascular inflammation, an increase in extracellular matrix deposition, and adventitial fibrosis. All of these processes cumulatively contribute to the progressive obliteration of the precapillary vessels, leading to an increase in pulmonary arterial pressure, right ventricular hypertrophy (RV), dysfunction, and death. The RV is the major determinant of functional state and prognosis in PAH. Plentiful molecular mechanisms contribute to the development of PAH and RV failure, including, in particular, an imbalance of vasoactive mediators, increased secretion of cytokines and chemokines, modulation of the activity of various growth factors, mitochondrial dysfunction, and changes in membrane receptors and ion channels. This Special Issue focuses on molecular mechanisms in PAH and RV hypertrophy and failure. We cordially welcome submissions, including original papers and reviews, on this broad topic.

Dr. Tatyana Novoyatleva
Dr. Akylbek Sydykov
Guest Editors

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• pulmonary hypertension
• right ventricular hypertrophy
• right heart failure
• pulmonary arterial hypertension
• pulmonary vascular cells
• endothelial dysfunction
• adventitial fibrosis