Key result
Terguride targets vascular remodeling as a potential pulmonary arterial hypertension therapy in preclinical models.
Why the study?
The serotonin pathway is involved in the pathogenesis of pulmonary arterial hypertension, and current therapies primarily address vasoconstriction rather than early vascular remodeling.
Does terguride improve outcomes in pulmonary arterial hypertension?
Does terguride improve outcomes in pulmonary arterial hypertension?
Terguride shows preclinical promise as an antiremodeling therapy for pulmonary arterial hypertension by targeting the serotonin pathway.
Answers are grounded in this paper and cite their sources.
Terguride merits early-phase PAH trials; leaves open whether serotonin antagonism improves outcomes.
Introduction: The serotonin pathway was initially identified as a major player in the pathogenesis of a subset of anorexigen-induced pulmonary arterial hypertension (PAH). It has subsequently been shown to be involved in other forms of PAH. Areas covered: In preclinical experiments, terguride (an anatagonist of type 2 serotonin receptors) was found to reduce proliferation of smooth muscle cells and accumulation of collagen, and decrease pulmonary arterial pressure. Expert opinion: Most therapies currently available for PAH primarily tackle vasoconstriction and endothelial dysfunction, whereas vascular remodeling, which is an early pathogenic event in PAH development, is secondary. If terguride demonstrates a prominent antiremodelling effect in PAH, it could be used as a specific therapy for this rare disease.
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Sabina A Antoniu (2011) conducted a review in pulmonary arterial hypertension. Terguride was evaluated. Terguride, an antagonist of type 2 serotonin receptors, shows potential as a specific therapy for pulmonary arterial hypertension by targeting vascular remodeling in preclinical models.
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