心梗后心力衰竭因其较高的发病率和病死率，已成为一个亟须解决的临床难题。心梗后心脏纤维化是引起心室重塑从而导致心力衰竭的重要原因之一，其中炎症反应是诱导和促进纤维化形成的重要因素，而NLRP3炎症小体是促进炎症反应的关键分子。在我们前期研究中发现，抑制SUMO-1基因的表达可减少小鼠心梗后炎症因子的释放及心脏纤维化的发生发展，进一步研究提示SUMO-1可促进NLRP3炎症小体的激活，其作用机制可能是通过SUMO-1与NEK7分子相互作用实现的。据此，我们提出假说：SUMO-1可通过与NEK7分子在细胞核内相互作用，增强NLRP3的转录表达，并对NLRP3的启动子区组蛋白修饰产生影响，加快心梗后心脏纤维化的进展。本课题拟通过动物、细胞和临床病例深入研究这一机制，进一步明确SUMO-1在心梗后心脏纤维化过程中的作用机制，为临床治疗心梗后心力衰竭寻找新的突破口。

Heart failure after myocardial infarction has become an urgent clinical problem due to its high morbidity and mortality.Cardiac fibrosis after myocardial infarction is one of the important causes of ventricular remodeling leading to heart failure. Among them, inflammatory response is an important factor to induce and promote the formation of fibrosis, and NLRP3 inflammasome is a key molecule to promote inflammatory response.In our previous study, it was found that inhibiting the expression of SUMO-1 gene could reduce the release of inflammatory factors and the occurrence and development of cardiac fibrosis after myocardial infarction in mice. Further studies suggested that SUMO-1 could promote the activation of NLRP3 inflammasome, and the mechanism of action might be realized by the interaction between sumo-1 and NEK7 molecules. Accordingly, we hypothesized that SUMO-1 could enhance the transcriptional expression of NLRP3 and influence the histone modification of the promoter region of NLRP3 by interacting with NEK7 molecules in the nucleus, thus influencing histone modification in the promoter region of NLRP3 to accelerate the progression of myocardial fibrosis after myocardial infarction. This project intends to conduct in-depth research on this mechanism through animal, cell and clinical case research to further clarify the role of SUMO-1 in the process of cardiac fibrosis after myocardial infarction, so as to find a new breakthrough for the clinical treatment of heart failure after myocardial infarction.