ADMA/DDAH系统与脑白质疏松症的关系

脑白质疏松症(LA)是深部脑小血管病变(SVD)引起的弥漫性脑缺血,可导致脑白质区神经传导纤维脱髓鞘疾病,是脑损害的一个早期标志。一氧化氮(NO)是血管内皮舒张因子,由体内的一氧化氮合酶(NOS)催化产生。非对称性二甲基精氨酸(ADMA)是NOS的内源性竞争抑制物。ADMA增加使NO生成减少,导致血管内皮功能障碍。二甲基精氨酸二甲胺水解酶(DDAH)是内源性ADMA的主要代谢酶,是决定血浆ADMA浓度的关键因素。ADMA/DDAH通路可能通过血管内皮损伤机制影响LA。

Association of ADMA/DDAH pathways and leukoaraiosis

Leukoaraiosis (LA) is a nerve conduction fiber demyelinating disease in the brain white matter resulted from diffuse cerebral ischemia caused by cerebral small vessel disease (SVD). It is an early sign of brain damage. Nitric oxide (NO) is an endothelium-derived relaxing factor, and its production is catalyzed by nitric oxide synthase (NOS). Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NOS. Increase of ADMA reduces the production of NO, which then leads to vascular endothelial dysfunction. Dimethylarginine dimethylaminohydrolase (DDAH) is a main metabolic enzyme of endogenous ADMA, and key factor determining the plasma content of ADMA. ADMA/DDAH pathway may affect LA through the mechanism of vascular endothelial damage.