Crosstalk between mitochondrial dysfunction and endoplasmic reticulum stress in apoptosis: Implications for grass...

The rapid degradation of fish flesh quality during cold storage poses significant challenges for the aquatic food industry. This study investigated the molecular mechanisms underlying grass carp (Ctenopharyngodon idella) flesh degradation, focusing on mitochondrial dysfunction and endoplasmic reticulum (ER) stress. Using 4D proteomics, we identified key apoptotic pathways, including the activation of caspase-9 and the unfolded protein response (UPR), which highlighted the crosstalk between mitochondria and ER during cold storage. Results showed that mitochondrial dysfunction serves as the primary trigger of apoptosis, initiating cytochrome c release and caspase activation, while ER stress exacerbates apoptosis by amplifying these pathways. Treatment with cyclosporine A (CsA) stabilized mitochondrial membranes, reduced ER stress markers such as GRP78 and CHOP, and maintained the Bax/Bcl-2 ratio, significantly delaying apoptosis and preserving muscle integrity. These findings provide novel insights into cellular mechanisms of fish flesh deterioration and propose potential strategies for improving aquatic product preservation.