Apoptosis and its role in postmortem meat tenderness: A comprehensive review

Tenderness is considered a crucial attribute of postmortem meat quality, directly influencing consumers' preferences and industrial economic benefits. The degradation of myofibrillar proteins by endogenous enzymes within muscle fibers is believed to be the most effective pathway for meat tenderization. After animals are slaughtered and exsanguinated, there is a significant accumulation of reactive oxygen species (ROS), and a dramatic depletion of adenosine triphosphate (ATP) in muscle, leading to inevitable cell death. Caspases are activated in postmortem muscle cells, which disrupt the cell structure and improve meat tenderness through protein hydrolysis. In this review, we systematically summarized the three primary types of cell death studied in postmortem muscle: apoptosis, autophagy and necrosis. Furthermore, we emphasized the molecular mechanisms of apoptosis and its corresponding apoptotic pathways (mitochondrial apoptosis, death receptors, and endoplasmic reticulum stress) that affect meat tenderness during muscle conversion to meat. Additionally, factors affecting apoptosis were comprehensively discussed, such as ROS, heat shock proteins, calcium (Ca2+)/calpains, and Bcl-2 family proteins. Finally, this comprehensive review of existing research reveals that apoptosis is mainly mediated by the mitochondrial pathway. This ultimately leads to myofibrillar proteins degradation through caspase activation, improving meat tenderness. This review summarizes the research progress on postmortem muscle apoptosis and its molecular mechanisms in meat tenderization. We hope this will enhance understanding of postmortem meat tenderness and provide a theoretical basis for meat tenderization techniques development in the future.