Abstract
Voltage-dependent anion channel isoform 3 (VDAC3), a channel in the mitochondrial outer membrane, has been suggested to play a role in the regulation of ATP transport and Ca2+ homeostasis. These processes are regarded as important for spermatozoa motility. Accordingly, in previous years, mutations in the VDAC3-encoding gene were detected in spermatozoa with low motility from infertile patients. Therefore, it can be assumed that these mutations would cause alteration of the structure and/or charge of the VDAC3 channel. The review is focused on current knowledge about contribution of VDAC3 activity to human spermatozoa motility and morphology. We also discuss the possibility of designing new molecules that could specifically block the VDAC3 channel and consequently act as male contraceptives.
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Financial & competing interests disclosure
The work was supported by the research grant of National Science Centre, Poland, Grant Number 2017/26/D/NZ1/00075. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.