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高同型半胱氨酸血症是动脉粥样硬化的独立危险因子,但是其致病机制尚未完全阐明。本文将从体液免疫、单核巨噬细胞以及T细胞活性等几方面归纳总结同型半胱氨酸在心血管疾病中的免疫调节作用。同型半胱氨酸可以诱导单核细胞和T细胞分泌趋化因子和细胞因子,还可以直接刺激 B 细胞增殖及 IgG 分泌。此外,本文还总结了高同型半胱氨酸致炎作用的细胞内机制。同型半胱氨酸可以直接或间接导致氧化应激或者内质网应激,还可以降低一氧化氮的生物活性,影响包括S- 腺苷蛋氨酸和 S- 腺苷同型半胱氨酸的水平,从而导致心血管疾病的发生。
Homocysteinemia is an independent risk factor for atherosclerosis, but its pathogenesis has not been fully elucidated. This article will summarize the immunomodulatory effects of homocysteine in cardiovascular diseases from humoral immunity, monocyte-macrophage and T cell activity. Homocysteine can induce monocytes and T cells to secrete chemokines and cytokines, and can also directly stimulate B cell proliferation and IgG secretion. In addition, this article also summarizes the intracellular mechanism of hyperhomocysteine-induced inflammation. Homocysteine can directly or indirectly lead to oxidative stress or endoplasmic reticulum stress, but also can reduce the biological activity of nitric oxide, including S-adenosyl methionine and S-adenosyl homocysteine levels, Leading to the occurrence of cardiovascular disease.