Endocrine · 2026
lncRNA Gm10451 mediates β-cell functional impairment in type 1 diabetes through the miR-24-3p/G6PD axis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Jiao, Zhang Lihai, Wang Xianhe, Li Jiaxin, Kang Yuming
Аннотация
BACKGROUND: Pancreatic β-cell dysfunction underlies type 1 diabetes mellitus (T1DM) progression. Previous study showed that lncRNA Gm10451 is upregulated by high glucose and contributes to β-cell impairment, but its mechanism remains unclear.
METHODS: Interactions among Gm10451, miR-24-3p, and G6PD were validated by dual-luciferase assay and Ago2-RNA immunoprecipitation (Ago2-RIP). Expression was measured by RT-qPCR and Western blot. β-cell functions were evaluated by glucose-stimulated insulin secretion (GSIS), CCK-8, TUNEL, ELISA, and hyperglycemic clamp in 30 mM glucose-treated MIN6 cell and STZ-treated C57BL/6 mice (Control injected with citrate buffer).
RESULTS: Gm10451 was upregulated in diabetic models. Gm10451 acted as ceRNA to spomge miR-24-3p, which directly targeted G6PD. Overexpression of Gm10451 suppressed G6PD, aggravated oxidative/ER stress and inflammation, inhibited insulin secretion and promoted β-cell apoptosis. miR-24-3p mimic reversed these impairments.
CONCLUSION: Gm10451 promotes β-cell dysfunction via the miR-24-3p/G6PD axis, representing a poteniall therapeutic target for diabetes-related β-cell dysfunction.
METHODS: Interactions among Gm10451, miR-24-3p, and G6PD were validated by dual-luciferase assay and Ago2-RNA immunoprecipitation (Ago2-RIP). Expression was measured by RT-qPCR and Western blot. β-cell functions were evaluated by glucose-stimulated insulin secretion (GSIS), CCK-8, TUNEL, ELISA, and hyperglycemic clamp in 30 mM glucose-treated MIN6 cell and STZ-treated C57BL/6 mice (Control injected with citrate buffer).
RESULTS: Gm10451 was upregulated in diabetic models. Gm10451 acted as ceRNA to spomge miR-24-3p, which directly targeted G6PD. Overexpression of Gm10451 suppressed G6PD, aggravated oxidative/ER stress and inflammation, inhibited insulin secretion and promoted β-cell apoptosis. miR-24-3p mimic reversed these impairments.
CONCLUSION: Gm10451 promotes β-cell dysfunction via the miR-24-3p/G6PD axis, representing a poteniall therapeutic target for diabetes-related β-cell dysfunction.