免疫性血小板减少症患者血小板自噬异常及干预策略

Immune thrombocytopenia（ITP）is the most common clinical autoimmune bleeding disorder, which does serious harm to human health. The main clinical features are thrombocytopenia, platelet autoantibodies in vivo, and bone marrow megakaryocytes normal or increased. Various mechanisms of humoral and cellular immune dysfunction can cause destruction of platelets. Through lysosomal system, autophagy can clear and degrade damaged cell structures, aging organelles, biological macromolecules and other substances, which is an important mechanism for the maintenance of intracellular homeostasis, defense and normal growth control. The latest study found that autophagy plays an important role to maintain platelet function. But the changes of platelet autophagy and the role of platelet autophagy regulation in ITP occurrence and development, has not been elucidated. Combined with the latest developments and previous research, our research team proposed the hypothesis as follows: Platelet autophagy and abnormal of PI3K / Akt / mTOR regulation pathway may involve in the pathogenesis of ITP. Regulation of platelet autophagy will become effective intervention strategy in ITP.

免疫性血小板减少症（ITP）是临床最常见的自身免疫性出血性疾病，严重危害人类健康。ITP以血小板减少、体内出现血小板自身抗体、骨髓巨核细胞数正常或增多为主要临床特点。体液免疫和细胞免疫功能异常等多种机制均可引起血小板的破坏。自噬（autophagy）通过溶酶体系统，清除降解细胞内受损伤的细胞结构、衰老的细胞器、以及不再需要的生物大分子等物质，是维持细胞内环境稳定、防御及正常生长控制的重要机制。最新研究发现，自噬对于维持血小板功能有重要作用，但血小板自噬的改变以及调节在ITP发生、发展中的作用尚未阐明。本课题组结合最新进展和既往研究工作基础提出如下假说：血小板自噬及其调节通路PI3K/Akt/mTOR异常参与了ITP患者的发病机制；调节血小板自噬可能成为ITP有效地治疗干预策略。