Abstract

To the Editor: I have read with great interest the recent report by Liu1 concerning putative interactions between peroxisome proliferator-activated receptor (PPARγ) and 5-hydroxytryptamine 2B (5-HT2B) receptor in pulmonary arterial hypertension (PAH). Previous studies, including ours, demonstrated that 5-HT participates in PAH. A pathophysiological role of 5-HT2B receptors was supported by the increased 5-HT2B receptor expression in rodent lungs of hypoxia- or monocrotaline-induced PAH and corroborated by the genetic or pharmacological inactivation of 5-HT2B receptors that prevented PAH development.2 Other evidence already showed that the PPARγ agonist rosiglitazone was beneficial in preventing PAH, and PAH developed spontaneously in mice with smooth muscle cell- or endothelial cell-specific deletion of PPARγ.3 Previous studies showed that the rat fundus contraction was mediated via the 5-HT2B receptor …

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call