Hyperglycemic stress aggravates diabetic retinopathy and nephropathy by promoting cilium disassembly via a deacetylation- and methylation-mediated regulatory mechanism
· 2026-09-03 · 原文
DOI：10.1371/journal.pbio.3003975
by Jie Ran, Changfeng Wei, Yang Yang, Yufei Zhang, Guizhi Guo, Nan Ma, Long Yin, Hongjun Fan, Jingrui Li, Heng Guo, Renshuai Zhang, Runa Wang, Dengwen Li, Min Liu Primary cilia are essential microtubule-based sensory organelles, and their dysfunction has been increasingly linked to metabolic stress. However, the underlying molecular mechanisms remain poorly understood. Herein, we reveal that ciliary defects in retinal photoreceptors and renal tubules exacerbate tissue damage during the progression of diabetic complications. Under hyperglycemic stress, protein arginine methyltransferase 1 (PRMT1) and histone deacetylase 6 (HDAC6) are significantly upregulated in both retinal and renal tissues. Genetic ablation of either enzyme effectively preserves ciliary architecture and restores organ fu
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1. 人话版
by Jie Ran, Changfeng Wei, Yang Yang, Yufei Zhang, Guizhi Guo, Nan Ma, Long Yin, Hongjun Fan, Jingrui Li, Heng Guo, Renshuai Zhang, Runa Wang, Dengwen Li, Min Liu Primary cilia are essential microtubule-based sensory organelles, and their dysfunction has been increasingly linked to metabolic stress.
However, the underlying molecular mechanisms remain poorly understood.
2. 领域脉络
Herein, we reveal that ciliary defects in retinal photoreceptors and renal tubules exacerbate tissue damage during the progression of diabetic complications.
3. 机制拆解
Genetic ablation of either enzyme effectively preserves ciliary architecture and restores organ fu
4. 证据与数字
Under hyperglycemic stress, protein arginine methyltransferase 1 (PRMT1) and histone deacetylase 6 (HDAC6) are significantly upregulated in both retinal and renal tissues.
5. 反例与边界
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6. 跨领域连接与意外收获
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7. 可复用方法
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