ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2026
The role and mechanism of the miR-137 regulatory axis in diabetic retinopathy.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiabetic retinopathy (DR) is a leading cause of blindness, yet its molecular mechanisms are incompletely understood. This study aimed to investigate the role and regulatory mechanism of miR-137 in DR.
methodsA total of 176 participants were enrolled in this study, comprising 126 patients with DR and 50 healthy controls. According to standard criteria, the DR patients were categorized into non-proliferative (NPDR, n = 111) and proliferative (PDR, n = 15) groups. Clinical parameters and serum miR-137 expression levels were measured in all subjects. In vitro, a high-glucose (HG) model was established using HRCECs. Transfection, inhibitor treatments, and target validation (dual-luciferase assay, rescue experiments) were employed to assess miR-137's role in oxidative stress, ferroptosis, inflammation, and its target gene Integrin α5 (ITGA5).
resultsClinically, serum miR-137 was significantly downregulated in DR patients (0.65 ± 0.05 vs. 0.99 ± 0.10, p < 0.001), negatively correlating with HbA1c, FBG, and LogMAR scores, and identified as a factor associated with proliferative DR progression. In vitro, HG suppressed miR-137 via ferroptosis, while miR-137 overexpression alleviated HG-induced oxidative stress, ferroptosis, and inflammation. ITGA5 was confirmed as a direct target of miR-137, and its overexpression reversed the protective effects of miR-137 mimic.
conclusionThis study reveals that miR-137 exerts a protective role in DR. Its downregulation disinhibits ITGA5, driving oxidative stress, ferroptosis, and inflammation, thereby exacerbating retinal microvascular damage.
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