白细胞分化抗原36（CD36）具有转运脂肪酸和介导炎症的“双重作用”。非酒精性脂肪性肝炎（NASH）中CD36表达异常增高，然而其原因不甚清楚。丝氨酸富集剪接因子3（SRSF3）具有剪接和转运mRNA以及调节翻译等功能。我们前期工作发现高脂条件下CD36表达增强，SRSF3含量减少，提示我们SRSF3与CD36表达存在负相关关系；炎症状态下CD36翻译效率提高，提示我们该过程可能与SRSF3的翻译调节功能相关。我们推测：肝脏SRSF3可能在翻译层面调节CD36蛋白的表达。本项目拟通过体内外实验，研究NASH中SRSF3调节mTOR/4E-BP1/eIF4E信号通路和SRSF3与CD36 mRNA 5’-UTR结合的具体分子机制，阐明SRSF3通过上述两条途径调节CD36的翻译，为明确NASH中CD36含量异常增高的原因和探寻NASH患者的防治策略提供理论依据。

Cluster of differentiation 36 (CD36) is involved in the occurrence and development of nonalcoholic steatohepatitis (NASH) by transporting fatty acids and mediating inflammation. However, little is known about the reason of abnormal CD36 expression in NASH. Serine-rich splicing factor 3 (SRSF3) functions in alternative splicing, nuclear export and translational control. We have found in the preliminary work that increased CD36 expression was coupled with decreased SRSF3 in a high-fat condition. This suggests that SRSF3 is negatively correlated with CD36 expression. CD36 translational efficiency was significantly increased under inflammatory conditions. This suggests that this process may be closely related to the role of SRSF3 in translation. We speculate that SRSF3 regulates the expression of CD36 at the level of translation. We design experiments in vivo and vitro to investigate the mechanism underlying the effect of SRSF3 on CD36 translation via mTOR/4E-BP1/eIF4E signaling pathway and the translation inhibition caused by SRSF3 binding to CD36 mRNA 5'-UTR. This study will provide reliable theoretical basis for clarifying the reasons for the abnormal increase of CD36 in NASH and exploring the prevention and treatment strategies of NASH.