American journal of translational research · 2026
Downregulation of miR-130b-3p is associated with the progression of type 2 diabetic nephropathy.
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Hua Xukai, Zhu Xiaoyan, Wu Jianzhuo, Zhang Hongbin
Аннотация
OBJECTIVE: To investigate the association between miR-130b-3p and the progression of type 2 diabetic nephropathy (T2DN) and the underlying mechanisms.
METHODS: A total of 279 patients with T2DN were enrolled and divided into the normal albuminuria (NAU) group (n=117), microalbuminuria (MIAU) group (n=98), and the macroalbuminuria (MAAU) group (n=64). Additionally, 80 healthy subjects were selected as the control group. The expression of miR-130b-3p was measured in each group, and the clinical biochemical parameters were recorded. A diabetic nephropathy (DN) rat model was established to further analyze the relationship between miR-130b-3p expression and the Bcl-2/Bax pathway.
RESULTS: The relative expression level of miR-130b-3p was significantly decreased in patients with type 2 diabetic nephropathy (T2DN). Moreover, its expression in patients of the MAAU group was notably lower than that in patients of the MIAU group. miR-130b-3p in T2DN patients was substantially negatively correlated with the course of disease, HbA1c, HOMA-IR, triglycerides, eGFR, TGF-β1 and TNF-α. Receiver operating characteristic (ROC) curve analysis demonstrated the diagnostic value of miR-130-3p for DN, with an area under the curve (AUC) of 0.854. Compared with the control group, the expression of miR-130b-3p and Bcl-2 in renal tissues of rats in the DN model group was significantly decreased, while the expression of Bax and caspase-3 was significantly increased. Additionally, the number of apoptotic cells in the renal cortex of rats in the DN model group was significantly higher than that in the control group.
CONCLUSION: Downregulation of miR-130b-3p in T2DN patients may reflect early renal injury in DN. Its underlying mechanism may involve the induction of apoptosis through the mitochondrial pathway activation, mediated by Bcl-2/Bax imbalance.
METHODS: A total of 279 patients with T2DN were enrolled and divided into the normal albuminuria (NAU) group (n=117), microalbuminuria (MIAU) group (n=98), and the macroalbuminuria (MAAU) group (n=64). Additionally, 80 healthy subjects were selected as the control group. The expression of miR-130b-3p was measured in each group, and the clinical biochemical parameters were recorded. A diabetic nephropathy (DN) rat model was established to further analyze the relationship between miR-130b-3p expression and the Bcl-2/Bax pathway.
RESULTS: The relative expression level of miR-130b-3p was significantly decreased in patients with type 2 diabetic nephropathy (T2DN). Moreover, its expression in patients of the MAAU group was notably lower than that in patients of the MIAU group. miR-130b-3p in T2DN patients was substantially negatively correlated with the course of disease, HbA1c, HOMA-IR, triglycerides, eGFR, TGF-β1 and TNF-α. Receiver operating characteristic (ROC) curve analysis demonstrated the diagnostic value of miR-130-3p for DN, with an area under the curve (AUC) of 0.854. Compared with the control group, the expression of miR-130b-3p and Bcl-2 in renal tissues of rats in the DN model group was significantly decreased, while the expression of Bax and caspase-3 was significantly increased. Additionally, the number of apoptotic cells in the renal cortex of rats in the DN model group was significantly higher than that in the control group.
CONCLUSION: Downregulation of miR-130b-3p in T2DN patients may reflect early renal injury in DN. Its underlying mechanism may involve the induction of apoptosis through the mitochondrial pathway activation, mediated by Bcl-2/Bax imbalance.