Research progress on the role of NLRP3 inflammasome in the treatment of ischemia-reperfusion injury

Abstract

NOD-like receptor protein 3(NLRP3) inflammasome, as a protein complex that constitutes the innate immune system, can mediate inflammatory responses by regulating the maturation and release of IL-1β and IL-18, which are the basic for multiple pathological injury. A variety of injury factors generated during ischemia-reperfusion injury (I/RI) can activate the NLRP3 inflammasome, resulting in the excessive release of IL-1β and IL-18, which in turn leads to an inflammatory cascade to aggravate the damage of various tissues and organs. Inhibition of NLRP3 inflammasome activation has become an effective method to alleviate organ I/RI. Therefore, exploring the detailed mechanism of NLRP3 inflammasome-mediated I/RI can provide a theoretical basis for the prevention and treatment of organ I/RI