Decoding the Regulatory Mechanism of Astaxanthin on Autophagy: Insights for Anti-Inflammatory Intervention.
- 2026-03-23
- Biomolecules 16(3)
- Li Feng
- Ming Yu
- Xiao Ma
- Peixi Qin
- Yi Zhang
- PubMed: 41897412
- DOI: 10.3390/biom16030477
Study Design
- Type
- Review
Autophagy is a crucial process for cellular self-regulation and renewal. Upon exposure to stress, membrane structures-primarily derived from the endoplasmic reticulum and mitochondria, with contributions from the plasma membrane-drive autophagosome biogenesis. This process begins with the formation of a cup-shaped phagophore, which elongates to sequester cytoplasmic cargo, closes to form an autophagosome, and ultimately fuses with lysosomes to create an autolysosome where degradation and recycling occur. This regulated process plays a vital role in maintaining cellular homeostasis, the pathogenesis of various diseases, and modulation of inflammation. Astaxanthin (AST), a carotenoid produced by microalgae, various microorganisms and marine organisms, possesses a unique chemical structure that endows it with significant biological activities, including potent antioxidant and anti-inflammatory properties. Emerging evidence, primarily from preclinical studies, suggests that AST modulates autophagy by regulating signaling pathways such as Reactive Oxygen Species (ROS)/Mitogen-activated Protein Kinase (MAPK) and interacting with nuclear factor erythroid 2-related factor 2(Nrf2)-mediated antioxidant responses, thereby influencing inflammatory balance. This review systematically elucidates how AST acts as a key "molecular modulator" in animal or cellular models, dynamically regulating autophagy to restore cellular homeostasis and thereby influencing the course and outcome of inflammation. Furthermore, we explore the autophagy-mediated anti-inflammatory effects of AST across different organ systems and discuss its preliminary clinical translational potential and future challenges, aiming to provide a concise and forward-looking roadmap for this promising research field.