Autophagy in Aquatic Animals: A Double‐Edged Sword in Environmental Stress Response and Nutritional Mitigation Strategies

ABSTRACT

The intensification of aquaculture and global climate change expose aquatic animals to multifaceted environmental stressors, triggering diverse stress‐response cascades to mitigate cellular damage and preserve physiological homeostasis. Autophagy, an evolutionarily conserved lysosome‐dependent catabolic process that degrades damaged or redundant cellular components to maintain cellular homeostasis and physiological functions, plays a crucial role in the environmental stress response in aquatic animals. This review systematically summarizes the modulatory influence of major environmental stressors (physical, chemical, and biological) on autophagic activity in aquatic species. Overall, the regulatory network mainly centers on oxidative stress responses, mitochondrial quality control, the 5′‐adenosine monophosphate‐activated protein kinase (AMPK)/mechanistic target of rapamycin kinase complex 1 (mTORC1) signaling axis, mitogen‐activated protein kinase (MAPK) cascade, endoplasmic reticulum (ER) stress and related pathways. The dynamic equilibrium of autophagic flux dictates the cellular fate balance between adaptive survival and stress‐induced injury: physiologically moderate autophagy functions as a cytoprotective and adaptive mechanism that confers stress resilience, whereas dysregulated autophagy (either impaired flux or excessive activation) disrupts cellular homeostasis and shifts cell fate toward apoptotic death. Additionally, this review explores the potential of nutritional intervention strategies to modulate autophagic activity and alleviate stress‐induced damage in aquatic animals. Finally, key challenges and prospective research directions are proposed, providing a theoretical framework for deciphering stress resistance mechanisms in aquatic animals and advancing sustainable aquaculture practices.