BMC endocrine disorders · 2026
The role of serum miR-28-5p in predicting diabetic retinopathy onset in type 2 diabetes.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Li Junli, Zhou Yijun, Wei Lichun, Zhao Yan, Wu Min, Li Chunjian
Аннотация
BACKGROUND: This research investigates miR-28-5p in type 2 diabetes mellitus (T2DM), aiming to clarify its mechanistic role and clinical significance in the pathogenesis of diabetic retinopathy (DR).
METHODS: The research enrolled 112 T2DM patients (including 58 non-DR (NDR) and 54 DR) and 72 healthy controls. The expression of miR-28-5p and RAP1B were assessed by quantitative reverse transcription polymerase chain reaction. Receiver operating characteristic curve was employed to determine the diagnostic value of miR-28-5p in DR. Cell proliferation and migration were determined using cell counting kit-8 assay and Transwell assay. Concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified via enzyme-linked immunosorbent assay. The direct targeting of RAP1B by miR-28-5p was validated using a luciferase reporter assay. The correlation between their expression was evaluated using Pearson correlation analysis.
RESULTS: In serum and cell samples, miR-28-5p was upregulated, while RAP1B was downregulated. In patients with DR, miR-28-5p expression was negatively correlated with that of RAP1B. miR-28-5p had good diagnostic value for distinguishing DR from NDR, with an area under the curve of 0.891, achieving a sensitivity of 77.80% and a specificity of 93.10% at a cut-off value of 2.165. In high-glucose (HG)-treated cells, inhibition of miR-28-5p enhanced cell proliferation and migration, while reducing IL-6 and TNF-α levels. RAP1B was a target gene of miR-28-5p. Suppressing miR-28-5p upregulated RAP1B in HG-treated cells.
CONCLUSIONS: miR-28-5p contributes to DR pathology by directly targeting and downregulating RAP1B. It may serve as a potential diagnostic biomarker and promising therapeutic target for DR.
CLINICAL TRIAL NUMBER: Not applicable.
METHODS: The research enrolled 112 T2DM patients (including 58 non-DR (NDR) and 54 DR) and 72 healthy controls. The expression of miR-28-5p and RAP1B were assessed by quantitative reverse transcription polymerase chain reaction. Receiver operating characteristic curve was employed to determine the diagnostic value of miR-28-5p in DR. Cell proliferation and migration were determined using cell counting kit-8 assay and Transwell assay. Concentrations of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were quantified via enzyme-linked immunosorbent assay. The direct targeting of RAP1B by miR-28-5p was validated using a luciferase reporter assay. The correlation between their expression was evaluated using Pearson correlation analysis.
RESULTS: In serum and cell samples, miR-28-5p was upregulated, while RAP1B was downregulated. In patients with DR, miR-28-5p expression was negatively correlated with that of RAP1B. miR-28-5p had good diagnostic value for distinguishing DR from NDR, with an area under the curve of 0.891, achieving a sensitivity of 77.80% and a specificity of 93.10% at a cut-off value of 2.165. In high-glucose (HG)-treated cells, inhibition of miR-28-5p enhanced cell proliferation and migration, while reducing IL-6 and TNF-α levels. RAP1B was a target gene of miR-28-5p. Suppressing miR-28-5p upregulated RAP1B in HG-treated cells.
CONCLUSIONS: miR-28-5p contributes to DR pathology by directly targeting and downregulating RAP1B. It may serve as a potential diagnostic biomarker and promising therapeutic target for DR.
CLINICAL TRIAL NUMBER: Not applicable.