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Pulmonary hypertension (PHTN) remains a disease with high morbidity and mortality and no known cure. The World Health Organization has categorized PHTN into 5 clinical classifications, as follows: (1) pulmonary artery hypertension; (2) PHTN with left heart disease; (3) PHTN with respiratory disease; (4) PHTN caused by chronic thrombotic/embolic disease; and (5) miscellaneous PHTN.1 Despite the broad and varied nature of these clinical conditions, PHTN presents with similar clinical pathological changes in the lung, including altered vasoreactivity, endothelial dysfunction, vascular intimal and medial remodeling, activation of inflammatory processes, and platelet activation. If untreated, these changes lead to right heart stress, failure, and death.1 At the cellular level, enhanced vasoconstriction, endothelial dysfunction, and endothelial cell and vascular smooth muscle cell (VSMC) proliferation are key components of disease progression. This underlying pathology is associated with a plethora of molecular changes, eg, increased inflammatory cytokine expression and increased levels of oxidative stress, altered NO bioavailability, and increased growth factor expression. These molecular changes alter the balance of kinase cascades, cAMP, cGMP, and ρ that ultimately modulate K+ and Ca2+ channel function and expression, cytoskeletal organization, and cell cycle progression.Current treatment targets for PHTN include Ca2+ channel blockade, selective endothelin A receptor and dual endothelin receptor antagonism, prostanoid replacement, and phosphodiesterase inhibition.2 These treatments may be applied singularly or in combination to achieve therapeutic goals. Moreover, these therapies have had limited success and are often associated with unwanted adverse effects, including systemic hypotension. The rapid rate of drug discovery for this condition …

Is Resveratrol the Magic Bullet for Pulmonary Hypertension?