Sepsis is a systemic inflammatory response syndrome caused by infection. The core mechanism underlying sepsis is immune dysfunction, with macrophages, as important cells of the innate immune system, playing an essential role. Autophagy has been shown to be closely related to inflammation and immunity, and autophagy enhancement in sepsis can play a protective role by negatively regulating abnormal macrophage activation, modulating macrophage polarization phenotype, reducing activation of the inflammasome and release of inflammatory factors, and affecting macrophage apoptosis. However, excessive autophagy may also lead to autophagic death of macrophages, which further aggravates the inflammatory response. The mechanisms underlying these functions are relatively complex and remain unclear, but may be related to a variety of signaling pathways such as NF-κB, mTOR, and PI3K/AKT. The administration of drugs to assist in the regulation of macrophage autophagy has become a novel treatment for sepsis. The present review focuses on the role and the potential mechanisms of macrophage autophagy in sepsis.
Keywords: apoptosis; autophagy; immunity; inflammation; macrophage; polarization; sepsis.