Association of miR-671-3p expression with clinical efficacy and complications in hemodialysis patients.

Vascular calcification (VC) is a common and severe complication in hemodialysis patients, increasing the risk of major adverse cardiovascular events (MACE). This study aimed to explore the clinical value of miR-671-3p in hemodialysis patients and its regulatory role in VC. A total of 163 end-stage renal disease (ESRD) patients undergoing hemodialysis were enrolled, including 107 with VC and 56 without VC. Clinical data were used to evaluate the role of miR-671-3p in the diagnosis (ROC) and risk prediction (logistic regression) of VC and MACE. A high-phosphorus-induced human aortic smooth muscle cells (hASMCs) calcification model was established, and then cell viability (CCK-8), apoptosis rate (flow cytometry), calcium content, alkaline phosphatase (ALP) activity, and the levels of Runx2 and α-SMA were measured. Bioinformatics analysis and a dual-luciferase assay were employed to predict and validate the downstream target genes of miR-671-3p. miR-671-3p was downregulated in VC patients and showed high diagnostic value for VC. Its levels showed significant correlations with disease severity and could effectively predict the risk of MACE in VC patients. Overexpression of miR-671-3p markedly alleviated calcification-induced decreases in cell viability, increases in apoptosis and calcium content, upregulation of ALP and Runx2, and downregulation of α-SMA; however, this protective effect was reversed by overexpression of its downstream target FBXW2. miR-671-3p may serve as a promising candidate biomarker for diagnosing VC and predicting MACE in VC patients. miR-671-3p may attenuate the progression of VC by inhibiting calcification in hASMCs.