Chung-Ming Hsieh

TL;DR: The growth-promoting effect of homocysteine on vascular smooth muscle cells, together with its inhibitory effect on endothelial cell growth, represents an important mechanism to explain homocy steine-induced atherosclerosis.

TL;DR: It is shown that high-dose corticosteroids exert cardiovascular protection through a novel mechanism involving the rapid, non-transcriptional activation of endothelial nitric oxide synthase (eNOS) in wild-type mice.

TL;DR: The data suggest that in the absence of HO-1, cardiomyocytes have a maladaptive response to hypoxia and subsequent pulmonary hypertension.

TL;DR: Heme oxygenase-1 transgenic mice were protected from the development of both pulmonary inflammation as well as hypertension and vessel wall hypertrophy induced by hypoxia, suggesting an important protective function of enzymatic products of HO-1 activity as inhibitors of Hypoxia-induced vasoconstrictive and proinflammatory pathways.

TL;DR: RNA blot analysis and immunoblot experiments indicate that interleukin-1β induces VEGF gene expression in smooth muscle cells, which indicates that IL-1 β may accelerate the progression of atherosclerotic lesions by promoting the development of new blood vessels.