Monocyte-Mediated Inflammation Involves Immune Imbalance In The Pathogenesis Of Diabetic Cataracts

Diabetes increases the risk of cataract formation by fivefold. Studies suggest that immune factors are associated with cataract development; however, the potential mechanisms linking immune factors to diabetic cataracts remain unclear. In this study, we explored the potential changes in cytokines and the mechanisms of immune imbalance that may occur during the pathological process of diabetic cataracts from the perspectives of gene expression and cellular regulation.

Tianjin Medical University Eye Hospital, Tianjin, China

RNA sequencing was performed on lenses from diabetic rats and human PBMCs. Combined analysis of peripheral blood PBMCs and single-cell sequencing data from lenses was conducted to identify immune-related factors influencing cataract formation in diabetes, followed by experimental validation.

Transcriptomic analysis of lenses from diabetic rats and immunohistochemistry of human lens capsules revealed increased apoptosis of lens epithelial cells and abnormal proportions of immune cells in the diabetic group. Transcriptomic analysis of human PBMCs showed an elevated ratio of non-classical monocytes. Single-cell transcriptome analysis indicated differentiation of classical monocytes into non-classical monocytes in the diabetic group, with significant upregulation of TNF and IFNG signaling pathways. Experimental studies confirmed elevated levels of inflammation in the blood and ocular tissues of the diabetic group.

Diabetes alters the peripheral immune environment, leading to increased intraocular inflammatory responses and apoptosis of lens epithelial cells, thereby exacerbating cataract formation.