Possible involvement of the mesenchymal cell marker Meflin in angiogenesis promotion and fibrosis suppression after retinal injury

Pathological tissue remodeling, including choroidal neovascularization (CNV) and fibrosis, is central to the development of retinal diseases such as age-related macular degeneration (AMD); however, its underlying molecular mechanisms remain incompletely defined. In this study, we examined the intraocular expression patterns of Meflin, a mesenchymal stromal cell marker with anti-fibrotic properties, and evaluated its role in the pathophysiology of retinal diseases using a mouse model. In wild-type mice, Meflin expression was detected in the ciliary body, lens epithelium, retinal pigment epithelium, optic nerve meningeal cells, and choroidal perivascular fibroblasts. Lineage-tracing analysis using a Meflin reporter mouse line revealed accumulation of Meflin-lineage cells within laser-induced CNV lesions. Interestingly, adeno-associated virus-mediated overexpression of Meflin increased CNV volume in the acute phase of retinal injury but significantly suppressed subretinal fibrosis in the chronic phase. These findings suggest that Meflin promotes angiogenesis to support tissue repair and inhibits fibrosis after retinal injury in a temporally dependent manner, consistent with its previously reported roles in mouse models of cancer and other fibrotic diseases. These results improve our understanding of retinal disease pathology and highlight Meflin as a potential therapeutic target in diseases such as AMD.