Yiu-Fai Chen

TL;DR: The hypothesis that endogenous endothelin-1 plays a major role in hypoxic pulmonary vasoconstriction and/or hypertension, right heart hypertrophy, and pulmonary vascular remodeling is supported and it is suggested that endothelins-receptor blockade may be useful in the treatment of hypoxia-induced pulmonary hypertension humans.

TL;DR: Cellular/molecular mechanisms by which estrogen modulates injury-induced inflammation, growth factor expression, and oxidative stress in arteries and isolated vascular smooth muscle cells are reviewed, with emphasis on the role of estrogen receptors and the nuclear factor-kappaB (NFkappa B) signaling pathway.

TL;DR: These observations provide direct demonstration of adventitial fibroblast migration into neointima of arteries after endoluminal injury.

TL;DR: The data indicate that the sex difference in myointimal proliferation after vascular injury is estrogen dependent, and the responsiveness of this gene to balloon injury of the artery is more rapid and more robust in the male than in the female rat.

TL;DR: The findings of concomitant increases in gene transcript levels forET-1 and the ETA and ETB receptors in lung, but not in the great vessels or any other organ examined, are consistent with the hypothesis that increased ET-1 synthesis in the lung contributes to pulmonary vascular remodeling and the maintenance of chronic hypoxic pulmonary hypertension.