Key result
Novel PAH therapies targeting BMPR2, inflammation, and mitochondrial pathways advance across ongoing trials.
Why the study?
Despite targeted therapies, PAH remains a progressive disease with significant morbidity and mortality, creating an unmet need for therapies that target or reverse the underlying pathogenesis.
This review summarizes emerging therapeutic targets and novel interventional strategies aimed at modifying the underlying pathogenesis of pulmonary arterial hypertension.
Pulmonary arterial hypertension is a chronic, progressive disorder of the pulmonary vasculature with associated pulmonary and cardiac remodeling. PAH was a uniformly fatal disease until the late 1970s, but with the advent of targeted therapies, the life expectancy of patients with PAH has now considerably improved. Despite these advances, PAH inevitably remains a progressive disease with significant morbidity and mortality. Thus, there is still an unmet need for the development of new drugs and other interventional therapies for the treatment of PAH. One shortcoming of currently approved vasodilator therapies is that they do not target or reverse the underlying pathogenesis of the disease process itself. A large body of evidence has evolved in the past two decades clarifying the role of genetics, dysregulation of growth factors, inflammatory pathways, mitochondrial dysfunction, DNA damage, sex hormones, neurohormonal pathways, and iron deficiency in the pathogenesis of PAH. This review focuses on newer targets and drugs that modify these pathways as well as novel interventional therapies in PAH.
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Shah et al. (2023) conducted a review in Pulmonary Arterial Hypertension (PAH). Investigational targeted therapies was evaluated. Emerging therapeutic targets for pulmonary arterial hypertension, including BMPR2 signaling, inflammatory pathways, tyrosine kinases, and mitochondrial dysfunction, are currently undergoing intensive investigation in pre-clinical and clinical trials.
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