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Purpose <p>To 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.</p> Methods <p>This controlled study included a total of 60 semen samples collected from male patients between 2023 and 2024. Participants were categorized into asthenozoospermic (A, <i>n</i> = 30) and normozoospermic (N, <i>n</i> = 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.</p> Results <p>Sperm with preserved MMP were significantly reduced in the asthenozoospermic group (<i>p</i> &lt; 0.0001, d = 2.12). Elevated MDA (p &lt; 0.0001, d = 2.58) and AOPP (<i>p</i> &lt; 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 (<i>p </i>= 0.003, d = 1.38; <i>p</i> = 0.0003, r = 0.51, respectively), and a strong correlation was found between these two markers in both groups (N, <i>p </i>&lt; 0.0001; A, <i>p </i>= 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.</p> Conclusions <p>Asthenozoospermia 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.</p>

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The mitochondrial signature of sperm motility loss: a study of mitophagy and apoptosis in asthenozoospermia

  • 期刊论文

  • 发表日期：

    2026年4月11日

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  • Kübra Nur Uzun,
  • Adile Merve Baki,
  • Ayşe Altun Akpınar,
  • İlknur Keskin,
  • Şule Ayla

摘要

Purpose

To 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.

Methods

This 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.

Results

Sperm 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.

Conclusions

Asthenozoospermia 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.