Abstract：Objective: To explore the effect of LncRNA SNHG14 on high glucose (HG)-induced proliferation and fibrosis of glomerular mesangial cells (GMC) by regulating the miR-101-3p/SGK1 axis. Methods: The serum of patients with diabetic nephropathy (DN) (DN group) and healthy people (NC group) were collected. RT-qPCR was used to detect the expression of SNHG14, miR-101-3p, and SGK1 mRNA in serum. Human GMC (HGMC) was cultured and assigned into NG group, HG group, HG+SNHG14 knockdown control (si-NC) group, HG+SNHG14 knockdown (si-SNHG14) group, HG+si-SNHG14+miR-101-3p inhibitor (in-miR-101-3p) group, and HG+si-SNHG14+SGK1 overexpression plasmid (pcDNA-SGK1) group. RT-qPCR was used to detect the expression of SNHG14, miR-101-3p, and SGK1 mRNA in each group. CCK-8, cloning formation, immunofluorescence, and Western blot were used to detect HGMC proliferation and fibrosis in each group. The dual luciferase and RIP assays were used to detect the relationship between miR-101-3p and SNHG14 (or SGK1). Results: The expression levels of SNHG14 and SGK1 mRNA in serum of patients in DN group were higher than those in the NC group, while the expression of miR-101-3p was lower (P<0.05). Compared with the NG group, SNHG14 expression in the HG group was upregulated, accompanied by significantly increased cell proliferation activity (OD value, colony formation, Ki67-positive cell rate) and elevated expression of fibrosis markers (SGK1, α-SMA, FN, Col IV), while miR-101-3p expression was downregulated (P<0.05). Importantly, compared with the HG+si-NC group, knockdown of SNHG14 (HG+si-SNHG14 group) effectively reversed these HG-induced effects, significantly inhibiting cell proliferation and fibrosis (P<0.05). Furthermore, on the basis of SNHG14 knockdown, either inhibition of miR-101-3p (HG+si-SNHG14+in-miR-101-3p group) or overexpression of SGK1 (HG+si-SNHG14+pcDNA-SGK1 group) could significantly reverse the anti-proliferative and anti-fibrotic effects caused by SNHG14 knockdown (P<0.05). SNHG14 targeted and regulated the miR-101-3p/SGK1 axis(P<0.05). Conclusion: LncRNA SNHG14 promotes HG induced proliferation and fibrosis of GMC by inhibiting miR-101-3p and upregulating SGK1.
牛晓静, 叶寒露, 张利芳, 张建. LncRNA SNHG14调控miR-101-3p/SGK1轴对高糖诱导的肾小球系膜细胞增殖及纤维化的影响[J]. 河北医学, 2026, 32(1): 1-8.
NIU Xiaojing, YE Hanlu, ZHANG Lifang, et al. The Effect of LncRNA SNHG14 on High Glucose Induced Proliferation and Fibrosis of Glomerular Mesangial Cells by Regulating the miR-101-3p/SGK1 Axis. HeBei Med, 2026, 32(1): 1-8.
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2026, Vol. 32 
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