Table 1 The function of cuproptosis-related genes in spermatogenesis.

From: Cuproptosis and cuproptosis-related cell death and genes: mechanistic links to spermatogenic cell death

Gene

Function

FDX1

FDX1 reduces mitochondrial respiration and affects metabolism, which in turn affects spermatogenesis. FDX1 also affects spermatogenesis by impairing the function, decreasing the number of supporting cells and mesenchymal stromal cells, and by degenerating and necrotizing the vacuoles of spermatogenic cells.

GLS

GLS maintains spermatogenesis by controlling cellular redox homeostasis, eliminating excess ROS, and avoiding spermatocyte oxidative stress-induced apoptosis.

PDHA1

PDHA1 causes spermatogenic disorders by promoting CD4 + T cell infiltration and mitochondrial apoptosis pathways.

LIAS

LIAS provides energy for spermatogenesis by maintaining the activity of the PDH complex through lipoic acid. Lipoic acid avoids the accumulation of ROS, reduces oxidative stress in sperm cells and damage to the testicular microenvironment.

DLD

DLD may promote ROS generation and cause DNA damage, and promote apoptosis of spermatogenic cells.

MTF1

MTF1 inhibits the mitochondrial apoptosis pathway and maintains sperm viability and DNA integrity. MTF1 reduces double-stranded DNA breaks and S-phase arrest, inhibits cell death due to ROS production, and maintains spermatogenesis.

CDKN2A

CDKN2A causes cell cycle arrest in the G1 phase and cellular senescence, affecting spermatogenesis.

SLC31A1/CTR1

High expression of CTR1 specificity in the testis is essential for spermatogenesis.

DLAT

DLAT may be involved in the pathogenesis of spermatogenic disorders through metabolic regulation, oxidative stress, autophagy, and immune microenvironment.

DBT

It may affect the apoptosis of spermatogenic cells by adjusting the Bcl-2/Bax ratio and changing the stability of mitochondrial membranes.

ATP7A/ATP7B

Maintain the microenvironment required for spermatogenesis by precisely regulating copper homeostasis.

GCSH

May affect spermatogenesis by affecting the JAK-STAT signaling pathway.