中性粒细胞胞外诱捕网（NETs）在脓毒症凝血紊乱中发挥重要的作用，自噬是NETs形成的关键环节。我们近期发现LPS可上调MALAT-1这一炎症损伤调控新因子，后者可促进NETs形成，这与自噬相关蛋白ATG4B上调有关。预实验结果提示MALAT-1可结合miR-34c-5p并削弱后者对ATG4B表达的抑制作用。因而，我们推测：MALAT-1可能通过结合miR-34c-5p上调ATG4B增强自噬进而促进NETs并参与凝血紊乱。为此，我们将在临床样本上验证MALAT-1、miR-34c-5p、ATG4B、NETs之间的关联性；随后在细胞和动物模型中探讨MALAT-1吸附抑制miR-34c-5p及靶向调控ATG4B的分子机制；最后在动物模型中探讨MALAT-1通过促进NETs形成调控凝血紊乱的作用方式。本研究将从调控NETs形成的新角度探讨脓毒症凝血紊乱的机制，为脓毒症的防治提供新的思路。

The neutrophil extracellular traps (NETs) play an essential role in sepsis coagulopathy. Autophagy is the key component in mediating the formation of NETs. Long noncoding RNA (LncRNA) MALAT1 is a new factor regulating inflammatory injury. Recently, we found that LPS can promote NETs formation through up-regulating MALAT1 which may be related to the up-regulation of autophagy related protein ATG4B. Previous experimental results showed that MALA-1 could combine with mir-34c-5p to decrease the inhibition of ATG4B expression. Therefore, we supposed that MALAT1 combined with mir-34c-5p up-regulated ATG4B expression to enhance autophagy, then promoted NETs formation and involved in coagulation disorder in sepsis. To identify the hypothesis, we will firstly confirm the relation of MALAT1、miR-34c-5p、ATG4B and NETs in clinical sepsis samples. Then, we will study the mechanism of MALAT1accumulation to inhibit mir-34c-5p and regulation of ATG4B in cell and animal models. Finally, we will discuss the mechanism of coagulation disorder regulation of MALAT1 in animal model. These studiesmay provide novel target and strategy for the prevention and treatment of sepsis.