Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory disease, including ulcerative colitis (UC) and Crohn’s disease (CD). The abnormality of inflammatory and immune responses in the intestine contributes to the pathogenesis and progression of IBD. Autophagy is a vital catabolic process in cells. Recent studies report that autophagy is highly involved in various kinds of diseases, especially inflammation-related diseases, such as IBD. In this review, the biological characteristics of autophagy and its role in IBD will be described and discussed based on recent literature. In addition, several therapies for IBD through modulating the inflammasome and intestinal microbiota taking advantage of autophagy regulation will be introduced. We aim to bring new insight in the exploration of mechanisms for IBD and development of novel therapeutic strategies against IBD.

Gastrointestinal cancers are a group of cancers occurred in gastrointestinal tissues with high morbidity and mortality rate. Although numerous studies were conducted on the investigation of gastrointestinal cancers, the real mechanisms haven’t been discovered, and no effective methods of prevention and treatment of gastrointestinal cancers have been developed. Autophagy, a vital catabolic process in organisms, have been proven to participate in various mechanisms and signaling pathways, thus producing a regulatory effect on various diseases. The role of autophagy in gastrointestinal cancers remains unclear due to its high complexity. In this review, firstly, the biological features of autophagy will be introduced. Secondly, the role of autophagy in three popular gastrointestinal cancers, namely esophageal cancer, gastric cancer, and colorectal cancer will be described and discussed by reviewing the related literature. We aimed to bring novel insights in exploring the real mechanisms for gastrointestinal cancers and developing effective and efficient therapeutic methods to treat gastrointestinal cancers.

Multiple sclerosis (MS) is widely acknowledged as a chronic inflammatory autoimmune disorder characterized by central nervous system (CNS) demyelination and neurodegeneration. The hyperactivation of immune and inflammatory responses is recognized as a pivotal factor contributing to the pathogenesis and progression of MS. Among various immune and inflammatory reactions, researchers have increasingly focused on the inflammasome, a complex of proteins. The initiation and activation of the inflammasome are intricately involved in the onset of MS. Notably, the NLRP3 inflammasome, the most extensively studied member of the inflammasome complex, is closely linked with MS. This review will delve into the roles of the NLRP3 inflammasome in the pathogenesis and progression of MS. Additionally, therapeutic strategies targeting the NLRP3 inflammasome for the treatment of MS, including natural compounds, autophagy regulators, and other small molecular compounds, will be detailed in this review.