Figure 7.

Summary diagram of the possible mechanisms related to TXLNA function contributing to maintenance of the apoptotic balance during testicular phagocytosis. GC apoptosis induces a significant increase in TXLNA expression, which inhibits ubiquitination and degradation of ABCA1 via suppression of EGFR phosphorylation, and then facilitates phagocytic activity of SCs. Removal of defective GCs via SC phagocytosis is crucial for homeostasis maintenance during normal spermatogenesis. Conversely, ablation of TXLNA, which causes EGFR hyperphosphorylated during phagocytosis, may result in the disruption of the ubiquitination of ABCA1 protein and the inevitable ABCA1 instability, followed by an unusual inhibition of the SC phagocytosis. Disruption of SC phagocytotic function causes imbalance between GC death and development, and finally leads to dyszoospermia