Archives of biochemistry and biophysics · 2026
miR-543 targets NFAT5 in diabetic foot ulcer diagnosis and endothelial protection.
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Liu Jinhua, Cao Lifeng, Wang Xiaxia
Аннотация
BACKGROUND: Diabetic foot ulcer (DFU) lacks effective early diagnostic and therapeutic targets.
OBJECTIVE: To explore the expression, clinical value and mechanism of miR-543 in DFU.
METHODS: A total of 80 healthy population, 83 T2DM patients without foot ulcer, and 124 DFU patients were enrolled. Serum miR-543 and NFAT5 levels were measured by qPCR. Correlation, ROC, and logistic regression analyses were conducted. HUVECswere treated with high glucose (HG) to establish an injury model. Cell function assays, dual-luciferase reporter assay and rescue experiments were performed.
RESULTS: miR-543 was markedly downregulated and NFAT5 increased in DFU patients, with a strong negative correlation between the two. miR-543 showed good diagnostic value for DFU and was correlated with ulcer severity and ABI. In HG-induced HUVECs, miR-543 overexpression improved proliferation, migration and angiogenesis, and reduced inflammation. NFAT5 was verified as a direct target of miR-543, and its overexpression reversed the protective effects of miR-543.
CONCLUSION: miR-543 inhibits endothelial dysfunction by targeting NFAT5, thereby hindering the progression of DFU.
OBJECTIVE: To explore the expression, clinical value and mechanism of miR-543 in DFU.
METHODS: A total of 80 healthy population, 83 T2DM patients without foot ulcer, and 124 DFU patients were enrolled. Serum miR-543 and NFAT5 levels were measured by qPCR. Correlation, ROC, and logistic regression analyses were conducted. HUVECswere treated with high glucose (HG) to establish an injury model. Cell function assays, dual-luciferase reporter assay and rescue experiments were performed.
RESULTS: miR-543 was markedly downregulated and NFAT5 increased in DFU patients, with a strong negative correlation between the two. miR-543 showed good diagnostic value for DFU and was correlated with ulcer severity and ABI. In HG-induced HUVECs, miR-543 overexpression improved proliferation, migration and angiogenesis, and reduced inflammation. NFAT5 was verified as a direct target of miR-543, and its overexpression reversed the protective effects of miR-543.
CONCLUSION: miR-543 inhibits endothelial dysfunction by targeting NFAT5, thereby hindering the progression of DFU.