ArticleJournal of assisted reproduction and genetics2026
The mitochondrial signature of sperm motility loss: a study of mitophagy and apoptosis in asthenozoospermia.
Article in Journal of assisted reproduction and genetics, 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
purposeTo investigate whether mitophagy contributes to the pathophysiology of asthenozoospermia through its association with apoptosis and oxidative stress, and to elucidate potential mechanisms underlying impaired sperm motility.
methodsThis controlled study included a total of 60 semen samples collected from male patients between 2023 and 2024. Participants were categorized into asthenozoospermic (A, n = 30) and normozoospermic (N, n = 30) groups based on sperm motility, according to WHO criteria. The expression of ATG5 and cyt-c was examined using immunofluorescence and western blotting. Mitochondrial membrane potential (MMP) was measured with JC-1 dye, and oxidative stress markers (MDA and AOPP) were quantified in seminal plasma. Transmission electron microscopy was performed to evaluate mitochondrial ultrastructure.
resultsSperm with preserved MMP were significantly reduced in the asthenozoospermic group (p < 0.0001, d = 2.12). Elevated MDA (p < 0.0001, d = 2.58) and AOPP (p < 0.0001, r = 0.71) levels seen in asthenozoospermic group are indicative of increased oxidative stress. ATG5 and cyt-c expression levels were significantly higher in astehenozoospermic sperm (p = 0.003, d = 1.38; p = 0.0003, r = 0.51, respectively), and a strong correlation was found between these two markers in both groups (N, p < 0.0001; A, p = 0.0002). However, no significant correlation was found between mitophagy/apoptosis markers and oxidative stress levels. Ultrastructural examination revealed mitochondrial damage and autophagosome-like structures in asthenozoospermic samples.
conclusionsAsthenozoospermia is characterized by increased mitophagy and apoptosis independent of MDA and AOPP, suggesting impaired mitochondrial quality control as a potential mechanism for reduced sperm motility. These findings provide insights into the molecular basis of sperm dysfunction and support further research into mitochondrial-targeted strategies for managing asthenozoospermia.
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