特发性非梗阻性无精症严重影响着男性生殖健康，其病因尚不明确。目前认为生精阻滞是其重要发病机制之一。Piwil1是精子发生过程中的关键基因，其基因敲除小鼠模型表现为生精阻滞，该基因的表达受到多方因素的调控，但具体调控机制尚不情况。我们前期研究发现hsa_circ_0008822的表达与该疾病发生存在相关性，敲低该CircRNA可以提高miR-483-3p表达从而抑制Piwil1表达。基于前期实验，我们提出假说：hsa_circ_0008822表达下降引起对miR-483-3p的吸附能力下降从而下调Piwil1的表达导致特发性非梗阻性无精症生精阻滞。为验证该假说，本研究拟从体内、体外水平探究该CircRNA在此疾病中的功能；阐明该CircRNA调控Piwil1表达引起生精阻滞的机制；分析该CircRNA与特发性非梗阻性无精症显微取精结局的关系，为临床诊断与治疗该疾病提供参考指标与理论依据。

Idiopathic non-obstructive azoospermia is a disease which severely affects male reproduction system, however, the pathogenic mechanism remains unknown. Current studies suggest that spermatogenesis block maybe a cause of this disease. The Piwil1 is a key gene involved in the normal spermatogenesis, the gene knockout mice model is characterized by spermatogenic block. The expression of gene could be regulated by multiple factors, however the specific regulatory mechanism of this gene is unclear. Based on our previous research, we found that the hsa_circ_0008822/miR-483-3p/Piwil1 axis is associated with this disease, the knocking down of the hsa_circ_0008822 could rise the expression of miR-483-3p which then inhibit the gene Piwil1. With these results, we propose the following hypothesis: The decrease of hsa_circ_0008822 expression results in the decrease of miR-483-3p adsorption capacity and the downregulation of Piwil1 expression, leading to the occurrence of idiopathic non-obstructive azoospermia and spermatogenesis arrest. To validate this hypothesis, we designed in vitro and in vivo experiments to investigate the function of hsa_circ_0008822 in idiopathic non-obstructive azoospermia; Besides, we are going to reveal the specific mechanism of hsa_circ_0008822 in regulation gene Piwil1 and its association with the outcome of microdissection testicular sperm extraction in idiopathic non-obstructive azoospermia, which could provide reliable information for clinical diagnosis and treatment.