Retinal damage caused by ischemia, infection, or physical injury results in the degeneration or death of photoreceptor cells, as well as severe vision loss. No effective neuroprotective drugs are available in the clinic to restore damaged cells. Our research group has shown that intravenous transplantation of MSCs was effective in alleviating photoreceptor damage.
Other studies have shown that intravitreal injection of MSC-derived sEVs decreased photoreceptor apoptosis and protected visual function, a protective effect similar to that of MSCs. In vitro experiments have shown that MSC-derived sEVs can reduce retinal cell loss caused by thermal injury by downregulating MCP-1.
We have also recently shown that subretinal injection of MSC-derived sEVs showed a therapeutic effect in a rat retinal detachment model by inhibiting the secretion of inflammatory cytokines, reducing apoptosis, and activating autophagy.
In a rodent ischemia-reperfusion model, intravitreal injection of MSC-derived sEVs increased retinal functional recovery after ischemic injury. After intravitreal injection, a large number of sEVs were observed in the ischemic retina and were concentrated in RGCs and microglia. The injected sEVs could be detected in the vitreous humor for up to four weeks after administration.
