Genetic improvement of pork quality is one of the hot topics in pig germplasm innovation. Backfat thickness and intramuscular fat content are important indexes of meat quality. MiRNAs are becoming recognized as a crucial regulator of adipose development. Therefore, it is crucial to understand how miR-23b regulates fat metabolism at the molecular level. In the present study, Oil Red O staining, and Western blot were used to evaluate the effect of miR-23b on the differentiation of porcine preadipocytes. Dual-luciferase reporter gene assay, pulldown, and RIP were used to reveal the mechanism of miR-23b regulating cell differentiation. The findings demonstrated that miR-23b promotes the expression of adipogenic factors and increases the content of lipid droplets, thus promoting the differentiation of preadipocytes. Further research found that miR-23b can directly bind to the 3’UTR of SESN3 to regulate adipogenic differentiation. In addition, it was speculated that miR-23b controls cell differentiation by positively regulating the expression of ACSL4 in other ways. Here, we demonstrate that miR-23b promotes the differentiation of porcine preadipocytes by targeting SESN3 and promoting the expression of ACSL4. The present study is meaningful to the improvement of pork quality and the development of animal husbandry.

Circular RNA (circRNA) has a significant impact on the maturation of skeletal muscle, although their precise functions within this framework remain largely uncharted. This study presents an investigation of the regulatory effect of circAGGF1 on myogenesis in myoblasts, including the potential molecular mechanisms involved. It is revealed that circAGGF1 facilitates the differentiation of myoblasts into other states while simultaneously enhancing the manifestation of type I muscle fibers. In vivo investigations with mice revealed the promotion of skeletal muscle expansion and maturation by circAGGF1, bolstering its regenerative capacity. Mechanistically, circAGGF1 interacts with miR-199a-3p by acting as a sponge, promoting the subsequent expression of Fgf7. Furthermore, rescue experiments indicated a counteraction of the myogenesis induced by circAGGF1 overexpression by miR-199a-3p. To summarize, this research highlights the role played by circAGGF1 in the development of skeletal muscle, providing a valuable resource for enhancing our understanding of skeletal muscle biology.