Fucoidan for potentially treating amblyopia: Autophagy-associated targets and therapeutic mechanisms

Amblyopia is a pediatric disorder characterized by reduced visual acuity and remains a major pediatric health challenge. Currently, effective drug therapies for amblyopia are limited. Therefore, screening and exploring potential bioactive compounds are promising strategies for treating amblyopia. Fucoidan, extracted from marine rockweed, exhibits significant pharmacological properties via the regulation of autophagy, including neuroprotective benefits. Therefore, the present study aims to identify the neuroprotective targets and pharmacological mechanisms of fucoidan against amblyopia via autophagy. Using a network pharmacology approach, 8 core target genes were identified, including MTOR, PIK3CA, PTPN11, PIK3CB, PIK3CG, TLR4, PDGFRA, and FLT3. GO and KEGG pathway analyses highlighted the role of these targets in association with brain and neuronal axon development, by targeting the ephrin receptor and brain-derived neurotrophic factor-receptor signaling pathways. Furthermore, spatial docking simulations revealed that fucoidan exhibits effective docking affinity for PIK3CA, PTPN11, and PDGFRA. Collectively, these preclinical findings provide key evidence for the neuroprotective targets and pharmacological mechanisms of fucoidan against amblyopia by regulating autophagy, thus concluding that fucoidan may be a potential therapeutic agent for managing amblyopia. The findings of the current study were derived from a systematic bioinformatics analysis; however, additional experimental and pre-clinical studies are necessary to confirm these results.