Circ_HIPK3 Inhibits H2O2-Induced Lens Epithelial Cell Injury in Age-Related Cataract Depending on the Regulation of miR-495-3p/HDAC4 Pathway.

Age-related cataract (ARC) is one of the most common chronic diseases. Circular RNA (circ)_HIPK3 is reported to be involved in the advancement of ARC, but its molecular mechanism has not been clarified. Our study provides a new perspective on the clinical treatment of ARC. Our data showed that the expression levels of circ_HIPK3 and histone deacetylase 4 (HDAC4) were downregulated, while microRNA (miR)-495-3p level was increased in ARC tissues and H2O2-induced SRA01/04 cells. Functional experiments showed that circ_HIPK3 and HDAC4 overexpression could inhibit H2O2-induced lens epithelial cell apoptosis and fibrosis. In terms of mechanism, we found that circ_HIPK3 could sponge miR-495-3p, miR-495-3p could target HDAC4. Besides, we confirmed that circ_HIPK3 sponged miR-495-3p to positively regulate HDAC4. Additionally, miR-495-3p overexpression or HDAC4 knockdown reversed the inhibition effect of circ_HIPK3 on H2O2-induced lens epithelial cell injury. In conclusion, our data showed that circ_HIPK3 suppressed H2O2-induced lens epithelial cell injury by regulating miR-495-3p/HDAC4 axis. [ABSTRACT FROM AUTHOR]