Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy

Sepsis is an uncontrolled host response to infection, resulting in a clinical syndrome involving multiple organ dysfunctions. Cardiac damage is the most common organ damage in sepsis. Uncontrolled inflammatory response is an important mechanism in the pathogenesis of septic cardiomyopathy (SCM). NLRP3 inflammasome promotes inflammatory response by controlling the activation of caspase-1 and the release of pro-inflammatory cytokines interleukin IL-1 beta and IL-18. The role of NLRP3 inflammasome has received increasing attention, but its activation mechanism and regulation of inflammation in SCM remain to be investigated. Inflammasomes play a key role in the development and progression of innate immunity and immunoinflammatory diseases. It was found that NLPR3 inflammasomes are closely related to sepsis and septic cardiomyopathy (SCM) and can be involved in regulating SCM through cardiomyocyte inflammatory response and apoptosis, oxidative stress injury, calcium regulation, endoplasmic reticulum stress, mitochondrial dysfunction, and exosomes.image