Dysregulation of miR-302a-3p in diabetic nephropathy and its role in inflammatory response.

Background: This research aims to reveal the regulatory mechanism of miR-302a-3p in diabetic nephropathy (DN) and its role in inflammatory responses.

Methods: Serum samples were collected from DN patients and healthy controls, and RT-qPCR was employed to determine miR-302a-3p expression levels. The diagnostic value of this molecule in DN was evaluated through the receiver operating characteristic curve. A high-glucose condition was induced in HK-2 cells to establish an in vitro cell model. CCK-8 and flow cytometry were used to assess cell viability and apoptosis changes. ELISA was used to detect the levels of inflammatory factors, and the ROS assay kit was used to assess the level of ROS. The dual-luciferase reporter assay confirmed the targeted binding relationship between miR-302a-3p and FGF-16. Functional rescue experiments were conducted by knocking down FGF-16.

Results: The level of miR-302a-3p in the serum of patients with DN was significantly increased, and its area under the curve (AUC) for diagnosing DN was 0.9168. High glucose induced an upregulation of miR-302a-3p in HK-2 cells. Inhibiting miR-302a-3p significantly reversed high glucose-induced cell apoptosis and release of ROS and pro-inflammatory factors. miR-302a-3p directly targets and inhibits FGF-16. In HK-2 cells induced by high glucose, knocking down FGF-16 would eliminate the protective effect of miR-302a-3p inhibitor on the cells.

Conclusions: miR-302a-3p enhances inflammatory response, oxidative stress and cell apoptosis by targeting and inhibiting FGF-16, thereby promoting renal tubular damage in DN.