Autophagy in Silkworm Biology: Progress and Perspectives

Autophagy is an evolutionarily conserved catabolic process essential for cellular quality control, metabolic adaptation, and developmental programming. The silkworm has emerged as a compelling model organism for investigating autophagy due to its well-characterized genome, ease of genetic manipulation, and significant homology with human disease-related genes. This review synthesizes current advances in silkworm autophagy research across four interconnected domains: molecular regulatory mechanisms, developmental functions, stress-induced responses, and disease-related implications. The steroid hormone 20-hydroxyecdysone (20E) orchestrates autophagy during metamorphosis through transcriptional upregulation of autophagy-related genes (Atgs) and mTOR inhibition. AMPK acts as a key energy sensor, phosphorylating BmAtg1c upon 20E stimulation or starvation. Functionally, autophagy participates in tissue remodeling, silk gland degeneration, and fat-body metabolism during development. Upon pathogenic infections (BmNPV, BmCPV, microsporidia) or xenobiotic stresses (pesticides, heavy metals), autophagy exhibits context-dependent duality—often promoting pathogen replication while also contributing to host defense. The interplay between autophagy and apoptosis serves as a critical molecular switch determining cellular fate under stress conditions. Collectively, these findings establish the silkworm as a versatile platform for decoding autophagy regulatory networks and their physiological significance.