First 2022 Publication

We participated to the Special Issue "Ion Channels in Sperm Physiology 2.0" of the International Journal of Molecular Sciences by reviewing the mutations in ion transporters and channels genes leading to human asthenozoospermia. Additional clues from pharmacological and proteomics studies, as well as from KO animal models, were listed too. This genetic overview is also enriched by perspectives about potential applications in infertility therapy and male contraception.

To read the full review: https://www.mdpi.com/1422-0067/23/7/3926

Sperm Ion Transporters and Channels in Human Asthenozoospermia: Genetic Etiology, Lessons from Animal Models, and Clinical Perspectives
Cavarocchi, Emma and Whitfield, Marjorie and Saez, Fabrice and Touré, Aminata

International Journal of Molecular Sciences 23,  (2022)  

Sperm Ion Transporters and Channels in Human Asthenozoospermia: Genetic Etiology, Lessons from Animal Models, and Clinical Perspectives

In mammals, sperm fertilization potential relies on efficient progression within the female genital tract to reach and fertilize the oocyte. This fundamental property is supported by the flagellum, an evolutionarily conserved organelle that provides the mechanical force for sperm propulsion and motility. Importantly several functional maturation events that occur during the journey of the sperm cells through the genital tracts are necessary for the activation of flagellar beating and the acquisition of fertilization potential. Ion transporters and channels located at the surface of the sperm cells have been demonstrated to be involved in these processes, in particular, through the activation of downstream signaling pathways and the promotion of novel biochemical and electrophysiological properties in the sperm cells. We performed a systematic literature review to describe the currently known genetic alterations in humans that affect sperm ion transporters and channels and result in asthenozoospermia, a pathophysiological condition defined by reduced or absent sperm motility and observed in nearly 80% of infertile men. We also present the physiological relevance and functional mechanisms of additional ion channels identified in the mouse. Finally, considering the state-of-the art, we discuss future perspectives in terms of therapeutics of asthenozoospermia and male contraception.