弱精子症发病机制的研究进展

弱精子症是男性不育的主要原因之一，多由染色体异常、微生物感染、内分泌紊乱、精索静脉曲张和自身免疫等因素引起，目前仍有相当比例弱精子症的发病机制未明。精子鞭毛结构蛋白对维持精子正常形态和运动能力十分重要，微管相关蛋白Tektins和细胞骨架重要组成成分Septins等基因发生突变或表达量减少均可导致精子的运动能力下降；精子细胞内的Ca2+、Cl-等离子浓度影响精子内磷酸化级联反应，使精子不断适应外界环境变化并完成获能、顶体反应等重要生理功能；Catspers、富半胱氨酸分泌蛋白（CRISPs）等离子通道及离子通道调节蛋白的表达异常与弱精子症发病密切相关；线粒体内的氧化磷酸化反应为精子运动提供能量，氧化磷酸化酶和呼吸链基因突变以及线粒体相关微小RNA表达异常都可能降低精子的运动能力；另外，JAK-STAT信号转导通路与精子的发生相关，而线粒体介导的精子细胞凋亡通路也与精子活动力低下有关。现就弱精子症发病机制的最新研究进展进行综述。

Research Advances in Pathogenesis of Asthenozoospermia

Asthenozoospermia, one of the important factors of male infertility, is caused by multi-factors such as chromosomal abnormalities, microbial infections, endocrine disorders, varicocele and autoimmune factors, etc. However, the mechanism remains unclear in a considerable proportion of asthenozoospermia. Structural proteins on sperm flagella maintain sperm morphology and mobility. The gene mutation or decreased expression of Tektins, a microtubule-associated protein, and Septins, a cytoskeletal component, can decrease sperm motility. The intracellular phosphorylation cascades are affected by the concentrations of ions in sperm, such as Ca2+, Cl-, etc., which is vital for the sperm to adapt to the change of external environment and to the important physiological function such as capacitation and acrosome reaction. Abnormalities of ion channels and their regulators, Catspers and CRISPs, are related to asthenozoospermia. Oxidative phosphorylation in mitochondria is the source of energy for sperm movement. Gene mutations of oxidative phosphorylase and respiratory chain-related proteins, and abnormal expression of mitochondria-associated microRNAs, might result in the reduced sperm motility. Besides, JAK-STAT signaling pathway is involved in spermatogenesis, and mitochondria-mediated pathways of sperm cell apoptosis are also associated with the reduced sperm motility. This review is focused on the pathogenesis of asthenozoospermia.