LAUSR

MicroRNAs (miRNAs) have been demonstrated to be involved in various cellular biological processes. However, their impacts on apoptosis and oxidative stress in ovarian granulosa cells (GC) remain largely unknown. Here, we identified that miR‐30b was transcriptionally activated in sow GCs during follicular atresia or from an in vitro oxidative stress GC model, leading to the specific upregulation of miR‐30b‐3p, a highly conserved miRNA located within sow reproductive trait locus and predominantly expressed in the cytoplasm of GCs. Notably, miR‐30b‐3p levels in follicles were negatively correlated with the E2/P4 ratio and the SOD/MDA index. Functional analysis revealed that miR‐30b‐3p induced the apoptosis and drove oxidative stress in sow GCs. Mechanistically, miR‐30b‐3p inhibits the expression of SMAD3 (antiapoptotic factor) and SOD2 (antioxidant enzyme) by directly binding to their 3′‐UTR. Furthermore, restoration of SMAD3 and SOD2 expression effectively suppressed the proapoptotic and pro‐oxidative functions of miR‐30b‐3p. In addition, KLF5 specifically activates the transcription of miR‐30b in sow GCs by acting as a transcription factor, resulting in its upregulation during follicular atresia and under oxidative stress. More importantly, ROC analysis indicated that miR‐30b‐3p level in GCs can serve as an effective biomarker to evaluate follicular development and antioxidant capacity. Our findings elucidate the critical role of miR‐30b‐3p in regulating GC apoptosis and oxidative stress, as well as its functional targets and expression regularity, suggesting that inhibition of miR‐30b‐3p is a potential approach for maintaining follicular development, enhancing ovarian antioxidant, and improving sow fertility.