Key result
MSC-derived small extracellular vesicles carrying miR-125b-5p mitigated retinal blood-retina barrier impairment and prevented endothelial cell ferroptosis by inhibiting P53.
Why the study?
The effects of mesenchymal stem cells-derived small extracellular vesicles (MSC-sEVs) on endothelial dysfunction in diabetic retinopathy and the underlying mechanisms remained unclear.
Does delivery of MSC-sEVs carrying miR-125b-5p prevent endothelial cell ferroptosis and protect the blood-retina barrier in diabetic retinopathy models?
Does delivery of MSC-sEVs carrying miR-125b-5p prevent endothelial cell ferroptosis and protect the blood-retina barrier in diabetic retinopathy models?
MSC-derived sEVs carrying miR-125b-5p may offer a therapeutic approach for diabetic retinopathy by preventing endothelial cell ferroptosis via P53 inhibition.
Hypothesis-generating for MSC-sEVs in diabetic retinopathy; human trials required before any clinical consideration.
Progressive endothelial cell injury of retinal vascular is a vital factor in diabetic retinopathy (DR) pathogenesis. Mesenchymal stem cells-derived small extracellular vesicles (MSC-sEVs) showed beneficial effects on DR. However, the effects of MSC-sEVs on endothelial dysfunction of DR and the mechanism is still unclear. In this study, MSC-sEVs mitigated retinal blood-retina barrier (BRB) impairment in rats with streptozotocin (STZ)-induced DR by reducing ferroptosis in vivo and in vitro. MSC-sEVs miRNA sequencing analysis revealed that miR-125b-5p may mediate human retina microvascular endothelial cells (HRMECs) ferroptosis and P53 as a downstream target based on dual-luciferase reporter assays. Silencing miR-125b-5p in MSC-sEVs reversed the therapeutic effects of MSC-sEVs on rats with DR and advanced glycation end products (AGEs)-treated HRMECs. Additionally, overexpression of miR-125b-5p could diminish ferroptosis in HRMECs, and this effect could be effectively reversed by overexpressing P53. This study indicated the potential therapeutic effect of MSC-sEVs on vascular endothelial function maintenance and that the delivery of sEVs carrying miR-125b-5p could prevent endothelial cell ferroptosis by inhibiting P53, thereby protecting the BRB.
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Tong et al. (2025) studied Diabetic retinopathy. MSC-derived small extracellular vesicles (MSC-sEVs) carrying miR-125b-5p vs. Control / Silenced miR-125b-5p was evaluated on Retinal blood-retina barrier (BRB) impairment and ferroptosis. MSC-derived small extracellular vesicles carrying miR-125b-5p mitigated retinal blood-retina barrier impairment and prevented endothelial cell ferroptosis by inhibiting P53.
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