<p>This paper aimed to address the function of the MIAT/miR-130a-3p/Pdgfra axis in retinal microglia activation in chronic retinal hypoperfusion injury (CRHI) mice. CRHI mouse models were constructed through bilateral common carotid artery occlusion (BCCAO). MIAT, Pdgfra, and miR-130a-3p expression levels in retinal tissues and cells were assessed. The expression of genes linked to the Nlrp3 inflammatory vesicle pathway (Gsdmd, Asc, Tlr4, Casp1, and Casp8) was assessed. Serum contents of inflammatory cytokines IL-18 and IL-1β were determined. Iba-1/Casp1/Csdmd expression was tested. Moreover, the interplay between miR-130a-3p and MIAT, as well as associations between Pdgfra and miR-130a-3p were verified. MIAT and Pdgfra expression was enhanced and miR-130a-3p diminished in BCCAO mouse models. MIAT downregulation reduced IL-18 and IL-1β contents and repressed microglia activation in BCCAO mice, and histopathological results also displayed raised mouse retinal thickness and diminished apoptosis. Both inhibiting miR-130a-3p and overexpressing Pdgfra can reverse the delayed effects of MIAT interference on CRHI. MIAT regulates miR-130a-3p to stimulate the expression of Pdgfra, thereby further promoting retinal microglia activation in CRHI mice. This provides potential targets for the development of innovative treatment approaches for retinal disorders.</p> Graphical Abstract <p>Mechanism of the MIAT/miR-130a-3p/Pdgfra axis in retinal microglia in CRHI mice.</p> <p></p>