Abstract: 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.

Key words: Asthenozoospermia, Flagellin, Ion channels, Mitochondria, Signal transduction