SOX2-OT serves as a diagnostic and prognostic biomarker for hypertensive left ventricular hypertrophy by targeting miR-30d-5p.

This study aims to explore the clinical significance and underlying mechanism of long noncoding RNAs (lncRNAs) SOX2-OT in hypertensive left ventricular hypertrophy (LVH). Primary hypertensives without LVH (n = 182) and with LVH (n = 104) were enrolled. ROC curve evaluated its diagnostic value for hypertensive LVH. Patients were followed for five years. Kaplan-Meier and Cox analyses were conducted to assess the prognostic value and identify potential risk factors for adverse cardiovascular events (MACEs). An in vitro model of Ang II-induced cardiomyocytes was established. Cell proliferation and apoptosis were analyzed using CCK-8 and flow cytometry. RT-qPCR was employed to detect the levels of SOX2-OT, miR-30d-5p, RUNX1, hypertrophy markers (ANP, BNP, and β-MHC), and anti-hypertrophic markers (α-MHC and Serca2α). Patients with hypertensive LVH exhibited higher SOX2-OT, RUNX1, and lower miR-30d-5p expression. SOX2-OT effectively distinguished LVH patients from hypertensive controls, with a sensitivity of 80.77% and specificity of 92.31%. Elevated SOX2-OT was correlated with higher MACE risk and may be a severe predictive factor. Mechanistically, SOX2-OT or RUNX1 directly targets miR-30d-5p. SOX2-OT downregulation could mitigate the increase in Ang II-induced myocardial hypertrophy markers, lower anti-hypertrophic marker levels, suppress cell proliferation, and boost apoptosis. Conversely, decreased miR-30d-5p appears to partially reverse these effects. SOX2-OT is upregulated in hypertensive LVH with favorable diagnostic performance and is correlated with adverse cardiovascular event risk.