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111年11月24日(四)12:30於3樓和氣會議室舉辦「研究發想會」(限定院內同仁參加)

111年11月24日(四)12:30於3樓和氣會議室舉辦「研究發想會」,由國立台灣大學生理學科暨研究所 李宗玄教授主講:「不對稱二甲基精氨酸在粥狀動脈硬化之角色Role of Asymmetric Dimethylarginine (ADMA) in Atherosclerosis」

本次講座摘要:

Graduate Institute and Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan
Asymmetric dimethylarginine (ADMA) is a circulating endogenous inhibitor of endothelial nitric oxide synthase (eNOS) by competing with L-arginine as the substrate and inhibits NO bioavailability, leading to the endothelial dysfunction. ADMA levels are increased in patients with hypertension, hyperlipidemia, atherosclerosis, chronic heart failure, diabetes mellitus and chronic renal failure. Therefore, increased levels of ADMA have been suggested as a novel risk marker beyond traditional risk factors for endothelial dysfunction-related diseases. Two isoforms of dimethylarginine dimethylaminohydrolase (DDAH) are responsible for the metabolism of ADMA. DDAH-1 is predominately expressed in proximal tube kidney and in the liver, whereas DDAH-2 is the predominant isoform in vascular cells. Overexpression of DDAHs is reported to ameliorate the progression of cardiovascular diseases in experimental animals. Therefore, maintaining the homeostasis of the DDAH-ADMA system may be beneficial for the cardiovascular function and human health. Currently, however, the clinical reagents targeting the activity or expression of DDAHs are not available. In my lab, I and my team investigate the role and mechanisms of ADMA on the therapeutic efficacy of statins, cholesterol metabolism of macrophage-foam cells and hyperuricemia. Our findings suggest that ADMA limits the beneficial effect of statins, deregulates the cholesterol metabolism of macrophages and participates in the hyperuricemia-accelerated atherosclerosis. Overexpression of DDAH-2 in endothelial cells prevents the detrimental effects of ADMA on the atherosclerosis.