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在糖尿病白内障中,METTL16通过m6A-修饰的DKK1-介导的Wnt/β-catenin信号传输抑制镜片上皮细胞功能

Bei Zhang^1,2, Yahui Sun^1,2, Xiaohui Jiang^1,2

¹Eye Hospital and School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, China.

Investigative ophthalmology & visual science

|January 14, 2026

概括

甲基转移酶样蛋白16 (METTL16) 和N6-甲基氨酸 (m6A) 甲基化在糖尿病白内障中升高. 这项研究揭示了METTL16向Dickkopf-1 (DKK1),抑制透镜细胞的增殖和进展,为糖尿病白内障的发病提供了新的见解.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学
眼科医生眼科眼科

背景情况:

糖尿病白内障 (DCs) 是糖尿病的一个重要并发症,但其潜在的分子机制仍然不太清楚.
甲基转移酶样蛋白16 (METTL16) 是一种N6-甲基氨酸 (m6A) 甲基转移酶,其在DC中的作用以前没有被研究过.

研究的目的:

阐明METTL16在糖尿病白内障发展和进展中的作用.
研究METTL16影响糖尿病白内障发生的分子机制.

主要方法:

在DC前组织和高葡萄糖 (HG) 诱导的人类透镜上皮细胞 (HLEC) 中量化m6A甲基化水平.
西部斑点分析检测METTL16表达.
甲基化RNA免疫沉 (MeRIP),RNA稳定性测试和细胞功能评估 (增殖,迁移,细胞周期).

主要成果:

在DC组织和HG诱导的HLEC中观察到高METTL16表达和m6A甲基化水平.
发现METTL16通过Wnt/β-catenin通路准Dickkopf-1 (DKK1). 通过Wnt/β-catenin通路准Dickkopf-1 (DKK1). 发现METTL16通过Wnt/β-catenin通路准Dickkopf-1 (DKK1). 发现METTL16通过Wnt/β-catenin通路准Dickkopf-1 (DKK1). 发现METTL16通过Wnt/β-catenin通路准Dickkopf-1 (DKK1). 发现METTL16通过Wnt/β-catenin通路准Dickkopf-1 (DKK1) 通过Wnt/β-catenin通路准Dickkopf-1 (DKK1).
DKK1表达与β-catenin核转移有负相关性,影响HLEC的增殖,迁移和细胞周期进展. DKK1的抑制防止了HG诱导的镜头不透明.

结论:

METTL16-DKK1-Wnt/β-catenin轴在抑制HG诱导的HLECs的增殖,迁移和细胞周期进展方面发挥着至关重要的作用.
这些发现为糖尿病白内障的病变产生提供了新的表观遗传洞察力,突出了METTL16作为潜在的治疗点.

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