ArticleMolecular biology reports2026
LncRNASNHG12 regulates the development of diabetic nephropathy through miR-129-5p/IL6ST axis.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiabetic Nephropathy (DN) pathogenesis remains incompletely understood.
objectivesThis study aimed to explore the mechanistic function of long non-coding RNA (lncRNA) SNHG12 in the progression of DN. MATERIALS AND
methodsIn this study, 150 type 2 diabetes mellitus (T2DM) patients and 150 DN patients were recruited. Human kidney-2 (HK-2) cells were exposed to high glucose (HG) to establish a DN cell model. The target gene expression was assessed by reverse transcription quantitative real-time PCR (RT-qPCR), cell proliferation was evaluated using the Cell Counting Kit-8 (CCK-8) assay, cell apoptosis was determined by flow cytometry, inflammatory factor levels were measured by enzyme-linked immunosorbent assay (ELISA), and molecular interactions were confirmed through the RNA immunoprecipitation (RIP) and dual-luciferase reporter assay.
resultsIn DN patients, SNHG12 and interleukin 6 signal transducer (IL6ST) were significantly elevated, whereas miR-129-5p expression was down-regulated, indicating that SNHG12 may serve as a potential biomarker for the auxiliary diagnosis of DN. Multivariate regression analysis showed that SNHG12 was a risk factor for DN. Moreover, under HG conditions, silencing of SNHG12 promoted cell proliferation, inhibited apoptosis, and mitigated inflammatory responses, as well as attenuated fibrosis, reflected by decreased expression of transforming growth factor-beta 1 (TGF-β1) and alpha-smooth muscle actin (α-SMA). Furthermore, SNHG12 could directly bind to and regulate miR-129-5p, which in turn targeted the 3'UTR of IL6ST. Inhibition of miR-129-5p or overexpression of IL6ST partially reversed the protective effects of SNHG12 knockdown on cellular functions.
conclusionSNHG12 promoted the progression of DN by upregulating IL6ST expression through the sponging of miR-129-5p.
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