ArticleMolecular biomedicine2025
FK506 binding protein 12.6-mediated inhibition of sperm-specific calcineurin is essential for FK506-induced male infertility by disturbing the homeostasis of calcium and mitochondria.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Impaired sperm motility is a leading cause of male infertility. Studies indicated that FK506, an immunosuppressive drug, resulted in male mouse infertility or an overall decline in the fertilization capacity of male renal transplant recipients. However, the underlying mechanism is not fully elucidated. Here, we reported that the disruption of FK506 binding protein 12.6 (FKBP12.6) significantly alleviated FK506-induced male infertility in mice by restoring sperm motility and mitochondrial functions in immature sperm. Mechanically, we identified that the FK506-FKBP12.6 complex preferentially bound to the sperm-specific calcineurin, which is composed of a catalytic subunit (PPP3CC) and a regulatory subunit (PPP3R2). We revealed that FKBP12.6 deficiency reversed FK506-induced the elevated expression of Down syndrome critical region 1.1 (DSCR1.1, a calcineurin inhibitor) and the reduced expressions of PPP3CC and PPP3R2 in immature sperm. Additionally, we observed that FKBP12.6 deficiency remarkably improved FK506-induced the abnormality of Ca
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