Abstract
Inflammasomes are complex molecular formations located in cells and take incharge of regulating the body's immune defence against infectious agents and injury. The initiation of inflammasomes is followed by caspase-1 turning on and gasdermin D being cut, thereby starting a process called pyroptosis. The activation of this process is effective in killing the pathogens, however, prolonged activation of inflammasomes can end up causing long-term inflammation, destruction of tissues, and emergence of different disorders. Herein, the article describes the structure, activation, and functions of such important sensors as NLRP1, NLRP3, AIM2, and pyrin and discusses their involvement in pathogenesis of diseases as rheumatoid arthritis, type 1 diabetes, atherosclerosis, COVID-19, toxoplasmosis, and malaria. As it has been discovered, signalling of Inflammasomes can be either helpful or harmful, and depend on the sensor used, the cellular environment, the agent of infection, as well as the level and length of activation of the signalling pathway. NLRP3 is mainly responsible for non-infectious inflammation, while AIM2 and NLRP1 can be responsible for protection and inflammatory processes. Pyrin is sensitive to the changes in RhoA signalling changes related to viruses, while mutations of disease-causing MEFV gene could lead to the non-regulated activation. Therapeutic approaches directed towards interleukin-1 signalling, NLRP3 formation, functioning of caspase-1, and pyroptosis are effective, despite the fact that they suffer from poor specificity, species difference involved, and lack of clinical application. A detailed knowledge of the regulation of inflammasome and disease-specific signalling may lead to the creation of selective biomarkers.