Objective This study investigated the expression and diagnostic significance of LINC00861 in DN and explored its functional mechanisms in high glucose-induced cell damage. Methods We enrolled 285 participants: 92 healthy controls, 98 uncomplicated T2DM patients, and 95 DN patients. Serum LINC00861 and miR-378a-3p levels were measured via qRT-PCR. Correlations with clinical parameters were assessed using Pearson analysis. Logistic regression identified risk factors for DN progression, and ROC curves evaluated diagnostic accuracy. In vitro, LINC00861 was knocked down to assess its effects on proliferation, inflammation, and oxidative stress under high glucose. Targeting of miR-378a-3p was confirmed by dual-luciferase and RIP assays. Results The LINC00861 expression was significantly elevated in DN patients compared to T2DM and healthy controls, and correlated positively with FBG, HbA1c, and albuminuria, but negatively with eGFR. Multivariate analysis identified LINC00861 as an independent risk factor for DN. The AUC for distinguishing T2DM from DN was 0.918. miR-378a-3p expression was significantly lower in DN patients than in those with T2DM or healthy controls. LINC00861 silencing may alleviate HG induced aberrant proliferation, inflammatory responses, and oxidative stress, possibly via the regulation of miR-378a-3p. Conclusion The LINC00861 is upregulated in DN and may facilitate renal injury by sponging miR-378a-3p, indicating its potential as a diagnostic biomarker and therapeutic target.
Li et al. (Sun,) studied this question.