Inflammasome protein cascades are very crucial as endogenous defence mechanisms. Nevertheless, their deregulation usually exacerbates deleterious chronic diseases. It is a large multicomplex cytosolic protein that plays a vital role in the innate immune system, therefore, acting as a vital mediator in the pathogenesis of non-communicable diseases. Pro-inflammatory cytokines like IL-1β and IL-18 are produced as a result of inflammatory reactions triggered by key inflammasomes. Notably, rheumatoid arthritis is largely caused by inflammasomes, particularly NLRP1 and NLRP3, which cause excessive inflammation and tissue damage by releasing cytokines that promote bone resorption and cartilage degradation. The development of stroke is facilitated by the NLRP3 inflammasome, which promotes inflammation and neuroinflammation, both of which cause brain damage. The pathogenesis of hypertension are significantly influenced by inflammasomes, especially NLRP3, which promote oxidative stress and inflammation, which worsen high blood pressure, cause cardiac fibrosis, and contribute to vascular and renal dysfunction. In asthma, inflammasomes primarily cause tissue damage and airway inflammation by activating NLRP3, which in turn causes the release of IL-1β and IL-18. This activation worsens asthma symptoms like inflammation and airway hyperresponsiveness while also boosting immunological responses, especially in Th2 and Th17 cells. The mechanisms governing inflammasome construction and activation, as well as the possibility of targeting inflammasomes to treat a variety of disorders, have thus become the focus of more recent study.