Abstract: Unexplained recurrent spontaneous abortion（URSA） is also known as alloimmune recurrent abortion. It is suggested that the main pathogenesis of URSA is immune imbalance at the maternal-fetal interface, abnormal trophoblast invasion and abnormal placental angiogenesis. Existing studies have revealed the important role of SIRT1 gene in the field of reproduction and the regulation of immune diseases. However, there is still a lack of systematic and comprehensive research overview on the mechanism of SIRT1 in improving URSA. SIRT1 may affect oxidative stress and autophagy by regulating the acetylation process of histones and key transcription factors, thus participating in numerous feedback loops and networks of URSA occurrence and development. Finally, SIRT1 can play a role in regulating trophoblast cell invasion and maternal-fetal interface angiogenesis. At the same time, the production of proinflammatory cytokines is suppressed to improve the excessive maternal immune inflammatory response during pregnancy. The activity of SIRT1 determines its deacetylation ability, which is crucial for downstream pathways and protein stability. Therefore, improving its activity is of great significance for improving URSA. Studies have shown that metformin and resveratrol can activate SIRT1 and protect SIRT1 and its downstream target proteins, which may be potential therapeutic agents for URSA. Based on the function of SIRT1, this article reviews the potential role of SIRT1 in the pathogenesis of URSA and the exogenous drugs targeting SIRT1 activation, in order to provide reference for the prevention and treatment of URSA in clinical research.

Key words: unexplained recurrent spontaneous abortion（URSA）, sirtuin 1（SIRT1）, trophoblast cell, angiogenesis, immune