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Updated: Mar 15, 2026

Retinal Pathophysiological Evaluation in a Rat Model
Published on: May 6, 2022
RNCR3 knockdown inhibits diabetes mellitus-induced retinal reactive gliosis
Chang Liu1, Chao-Peng Li2, Jia-Jian Wang3
1Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China; Shanghai Key Laboratory of Visual Impairment and Restoration, Shanghai, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Abstract:
Retinal reactive gliosis is an important pathological feature of diabetic retinopathy. Identifying the underlying mechanisms causing reactive gliosis will be important for developing new therapeutic strategies for treating diabetic retinopathy. Herein, we show that long noncoding RNA-RNCR3 knockdown significantly inhibits retinal reactive gliosis. RNCR3 knockdown leads to a marked reduction in the release of several cytokines. RNCR3 knockdown alleviates diabetes mellitus-induced retinal neurodegeneration, as shown by less apoptotic retinal cells and ameliorative visual function. RNCR3 knockdown could also decrease Müller glial cell viability and proliferation, and reduce the expression of glial reactivity-related genes including GFAP and vimentin in vitro. Collectively, this study shows that RNCR3 knockdown may be a promising strategy for the prevention of diabetes mellitus-induced retinal neurodegeneration.
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