The formation of cellular autophagy and its effect on meat quality

Autophagy regulates lipid metabolism to maintain the balance of adipose tissues (Fat, including BAT and WAT) and modulates meat tenderness. Autophagy and apoptosis interact bidirectionally (mutually reinforcing): autophagy maintains metabolic homeostasis by degrading cellular components, while apoptosis activates caspase-3/9 and autophagy markers, jointly influencing post-slaughter muscle quality. Oxidative stress induces autophagy via ROS and directly promotes apoptosis. Post-slaughter ROS accumulation exacerbates oxidative stress, accelerating caspase-9 generation, thereby regulating lipid metabolism and meat attributes. BAT, brown adipose tissue; WAT, white adipose tissue; ROS, reactive oxygen species. Meat quality, primarily assessed by colour, flavour, tenderness and juiciness, is increasingly important as rising global incomes enhance consumer purchasing power and demand for higher-quality meat. Recent studies highlight the significant correlation between autophagy and meat quality, particularly concerning fat content and tenderness. Autophagy, a dynamic homeostasis process, regulates intracellular fat metabolism within adipose tissue. Furthermore, the destruction of muscle organelle and macromolecules post-slaughter promotes autophagic activity. Consequently, cellular autophagy has emerged as a key area of research in animal meat quality. This paper summarizes the regulatory mechanisms of cellular autophagy and reviews current research on its association with meat quality. In conclusion, autophagy enhances tenderness by promoting proteolysis and apoptosis pathways post-slaughter, while modulating fat deposition through lipophagy-mediated lipid metabolism, thereby offering a promising target for improving meat quality.