Inflammasomes are key regulators of innate immune responses, controlling the activation of caspase-1, which in turn processes pro-inflammatory cytokines IL-1β and IL-18, and induces pyroptosis. Inflammasomes recognize microbial and endogenous ligands through direct or indirect mechanisms, and their regulation is crucial to prevent excessive inflammation. Multiple regulatory mechanisms have been identified that control inflammasome signaling at various stages. The main inflammasomes include NLRP3, NLRC4, NLRP1, NLRP6, NLRP12, and PYHIN (AIM2 and IFI16) inflammasomes. NLRP3 is activated by diverse stimuli, including microbial and endogenous signals, while NLRC4 responds to bacterial flagellin and T3SS components. NLRP1 is activated by anthrax toxin, and NLRP6 and NLRP12 are involved in maintaining intestinal homeostasis. PYHIN inflammasomes recognize dsDNA and are activated by viral or bacterial DNA. Regulation of inflammasome activation involves various mechanisms, including microbial strategies to inhibit inflammasome signaling, type I interferons that modulate inflammasome activity, and autophagy that influences inflammasome function. Additionally, TRIM family proteins and POPs/COPs regulate inflammasome signaling. The regulation of inflammasome pathways is essential to prevent sterile inflammation and maintain immune homeostasis. Understanding these mechanisms is critical for developing therapeutic strategies for diseases involving inflammasome dysregulation.Inflammasomes are key regulators of innate immune responses, controlling the activation of caspase-1, which in turn processes pro-inflammatory cytokines IL-1β and IL-18, and induces pyroptosis. Inflammasomes recognize microbial and endogenous ligands through direct or indirect mechanisms, and their regulation is crucial to prevent excessive inflammation. Multiple regulatory mechanisms have been identified that control inflammasome signaling at various stages. The main inflammasomes include NLRP3, NLRC4, NLRP1, NLRP6, NLRP12, and PYHIN (AIM2 and IFI16) inflammasomes. NLRP3 is activated by diverse stimuli, including microbial and endogenous signals, while NLRC4 responds to bacterial flagellin and T3SS components. NLRP1 is activated by anthrax toxin, and NLRP6 and NLRP12 are involved in maintaining intestinal homeostasis. PYHIN inflammasomes recognize dsDNA and are activated by viral or bacterial DNA. Regulation of inflammasome activation involves various mechanisms, including microbial strategies to inhibit inflammasome signaling, type I interferons that modulate inflammasome activity, and autophagy that influences inflammasome function. Additionally, TRIM family proteins and POPs/COPs regulate inflammasome signaling. The regulation of inflammasome pathways is essential to prevent sterile inflammation and maintain immune homeostasis. Understanding these mechanisms is critical for developing therapeutic strategies for diseases involving inflammasome dysregulation.