ArticleFrontiers in endocrinology2026
CAPZA1 deficiency disrupts sperm flagellar structure and motility, potentially involving the p300/SLC7A11 pathway.
Article in Frontiers in endocrinology, 2026. 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
Objective: To investigate the genetic and molecular role of CAPZA1 in asthenozoospermia and its impact on sperm motility and flagellar integrity. Methods: Whole-exome sequencing (WES) was first performed in an infertile family with asthenozoospermia to identify candidate variants. The CAPZA1 variant was further screened by Sanger sequencing in 20 infertile men with asthenozoospermia and 20 age-matched fertile controls. CAPZA1 expression and sperm motility parameters were assessed by Western blot and computer-assisted semen analysis, respectively. Structural abnormalities were examined using transmission electron microscopy (TEM). Results: A rare homozygous missense mutation in CAPZA1 (c.11T>C, p.Phe4Ser) was first identified by WES in the proband of an infertile family and was subsequently detected by Sanger sequencing in 3 of 20 asthenozoospermic patients. CAPZA1 protein expression was significantly reduced in mutant sperm, with a strong positive correlation to progressive motility ( Conclusion: CAPZA1 deficiency impairs sperm motility and flagellar architecture through disrupted cytoskeletal protein regulation and redox imbalance, and represents a novel genetic contributor to asthenozoospermia.
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