Annals of medicine · 2026
Astrocyte exosomes shield retina from ischemia via CaMKII-autophagy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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He Dan, Li Hua, Wei Chunling, Chen Chen, Li Juanjuan
Аннотация
BACKGROUND: Retinal ischemia-reperfusion (RIR) injury impairs vision through microvascular damage and inflammation. While astrocyte-derived exosomes (ADEs) offer neuroprotection, their role in protecting retinal microvasculature is unclear. This study investigates ADEs' effects on retinal microvascular endothelial cells (RMECs) in RIR.
METHODS: ADEs were isolated from astrocytes. Mouse RIR and cellular oxygen-glucose deprivation/reoxygenation (OGD/R) models were used. We assessed ADEs' impact on retinal microcirculation, microglial activation, and RMEC function. The roles of neurogranin and the CaMKII-autophagy pathway were examined using inhibitors.
RESULTS: ADEs, rich in neurogranin, alleviated RIR-induced microvascular damage and suppressed OGD/R-triggered pro-inflammatory microglial activation. This was associated with increased neurogranin, CaMKII phosphorylation, and autophagy in microglia. Consequently, ADEs counteracted the harmful effects of activated microglia on RMEC proliferation, migration, and tube formation. Inhibiting CaMKII or autophagy blocked ADEs' protective benefits without altering neurogranin, placing the CaMKII-autophagy axis downstream.
CONCLUSION: ADEs protect RMECs from RIR injury by modulating microglial responses via a neurogranin-CaMKII-autophagy mechanism, revealing their therapeutic potential for retinal microvascular protection.
METHODS: ADEs were isolated from astrocytes. Mouse RIR and cellular oxygen-glucose deprivation/reoxygenation (OGD/R) models were used. We assessed ADEs' impact on retinal microcirculation, microglial activation, and RMEC function. The roles of neurogranin and the CaMKII-autophagy pathway were examined using inhibitors.
RESULTS: ADEs, rich in neurogranin, alleviated RIR-induced microvascular damage and suppressed OGD/R-triggered pro-inflammatory microglial activation. This was associated with increased neurogranin, CaMKII phosphorylation, and autophagy in microglia. Consequently, ADEs counteracted the harmful effects of activated microglia on RMEC proliferation, migration, and tube formation. Inhibiting CaMKII or autophagy blocked ADEs' protective benefits without altering neurogranin, placing the CaMKII-autophagy axis downstream.
CONCLUSION: ADEs protect RMECs from RIR injury by modulating microglial responses via a neurogranin-CaMKII-autophagy mechanism, revealing their therapeutic potential for retinal microvascular protection.