Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role ...Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role of theγ-hydroxybutyrate analog HOCPCA in a glaucoma model,focusing on its effects on CaMKII signaling,oxidative stress,and neuroinflammatory responses.Retinal tissue from high IOP animal models was analyzed via proteomics.In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress,followed by HOCPCA treatment.HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure,preserving neuronal function.It restored CaMKIIαandβlevels,preserving RGC integrity,while also modulating oxidative stress and neuroinflammatory responses.These findings suggest that HOCPCA,through its interaction with CaMKII,holds promise as a neuroprotective therapy for glaucoma.展开更多
基金The position of M.H.was funded by grants from the state of North-Rhine-Westphalia,Germany(AZ:323-8.04.10.02-141905)the German Center for Infection Research,DZIF(TTU 08.927 and TTU 08.928)+1 种基金the Deutsche Forschungsgemeinschaft(DFG),SFB 670 procured by Prof.Dr.Martin Krönkesupported by the Deutsche Forschungsgemeinschaft(DFG)with grants PR1569/1-1 and PR 1569/1-3.
文摘Neuronal injury in glaucoma persists despite effective intraocular pressure(IOP)control,necessitating neuroprotective strategies for retinal ganglion cells(RGCs).In this study,we investigated the neuroprotective role of theγ-hydroxybutyrate analog HOCPCA in a glaucoma model,focusing on its effects on CaMKII signaling,oxidative stress,and neuroinflammatory responses.Retinal tissue from high IOP animal models was analyzed via proteomics.In vitro mouse retinal explants were subjected to elevated pressure and oxidative stress,followed by HOCPCA treatment.HOCPCA significantly mitigated the RGC loss induced by oxidative stress and elevated pressure,preserving neuronal function.It restored CaMKIIαandβlevels,preserving RGC integrity,while also modulating oxidative stress and neuroinflammatory responses.These findings suggest that HOCPCA,through its interaction with CaMKII,holds promise as a neuroprotective therapy for glaucoma.
