NEAT1 Regulates Calcium Oxalate Crystal-Induced Renal Tubular Oxidative Injury MiR-130/IRF1

Calcium oxalate (CaOx) crystal deposition induces damage to the renal tubular epithelium, increases epithelial adhesion, and contributes to CaOx nephrocalcinosis. The long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 () is thought to be involved in this process. In this study, we aimed to investigate the mechanism by which regulates renal tubular epithelium in response to inflammatory and oxidative injury triggered by CaOx crystals. As CaOx crystals were deposited in mouse kidney tissue, the expression of was significantly elevated and positively correlated with interferon regulatory factor 1 (), Toll-like receptor 4 (), and . targets and inhibits as a competitor to endogenous RNA. binds to and exerts inhibitory effects on the 3'-untranslated region of . After transfected with silence-NEAT1, , , and were also variously inhibited, and oxidative damage in renal calcinosis was subsequently attenuated. When we simultaneously inhibited and , renal tubular injury was exacerbated. We found that the lncRNA can enhance IRF1 signaling through targeted repression of and activate TLR4/NF-κB pathways to promote oxidative damage during CaOx crystal deposition. This provides an explanation for the tubular epithelial damage caused by CaOx crystals and offers new ideas and drug targets for the prevention and treatment of CaOx nephrocalcinosis. 38, 731-746.