ArticleDiabetes2026
Deletion of 12/15-Lipoxygenase Preserves Retinal Thickness and Function and Selectively Restores Dysregulated miRNAs in Experimental Diabetes Mice.
Article in Diabetes, 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
Diabetic retinopathy (DR) remains a leading cause of blindness, characterized by progressive neurovascular dysfunction. While the enzyme 12/15-lipoxygenase (12/15-LO) and its metabolites are upregulated in DR, their interactions with epigenetic regulators, such as miRNAs, are poorly understood. This study investigates the role of 12/15-LO in miRNA dysregulation and its functional consequences in a type 1 diabetic mouse model. We generated 12/15-LO knockout mice on an (Ins2+/akita) (Akita) background. Retinal miRNA expression was profiled using microarray analysis, and retinal structure and function were assessed using histology and electroretinography. Our results demonstrate that diabetes induces significant dysregulation of a distinct subset of retinal miRNAs (e.g., downregulation of miR-329-3p and miR-431-5p and upregulation of miR-3078-3p and miR-323-5p). Deletion of 12/15-LO normalized a subset of these diabetes-associated miRNA alterations and prevented retinal thinning and the loss of neuronal markers (NeuN and SCGN). Functionally, 12/15-LO deletion rescued diabetes-induced deficits in retinal ganglion cell (positive scotopic threshold response), cone bipolar cell (photopic b-wave), and cone pathway function (response to natural noise). In conclusion, our findings establish 12/15-LO as a critical upstream regulator of miRNA in the diabetic retina and demonstrate that its deletion protects against neuronal damage in DR. Thus, targeting the 12/15-LO pathway may represent a novel therapeutic strategy to mitigate neuronal dysfunction associated with DR progression. ARTICLE HIGHLIGHTS: Retina of Akita diabetic mice demonstrated significant thinning and dysfunction. Deletion of 12/15-lipoxygenase (12/15-LO) in Akita diabetic mice, an essential enzyme that metabolizes arachidonic acid to 12- and 15-hydroxyeicosatetraenoic acids, restored normal retinal thickness and preserved retinal neurons and function. Deletion of 12/15-LO selectively restored essential mature forms of miRNA, such as miR431 and miR329, which are implicated in neuroprotection, synaptic plasticity, and cellular response to stress. Targeting 12/15-LO and its metabolites has the potential to protect retina against diabetes neurodegeneration.
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