Table 1. Key mechanisms of NLRP3 inflammasome activation.

S. N.	Activation mechanism	Description	Key triggers	References
1	Canonical pathway	Requires two signals: priming (via NF-κB) and activation (via danger signals)	PAMPs (LPS, bacterial toxins), DAMPs	28
2	Non-canonical pathway	Involves caspase-11 (mouse) or caspase-4/5 (human) activation by intracellular LPS	Intracellular Gram-negative bacteria	29
3	Efflux of potassium ions (K+)	Decrease in intracellular efflux of potassium ions triggers NLRP3 oligomerization	ATP-P2X7 receptor activation	30
4	Calcium (Ca2+) signaling	Increased cytosolic calcium (Ca2+) signaling enhances inflammasome activation	Endoplasmic reticulum stress, ionophores	31
5	Lysosomal rupture	Release of cathepsins and DAMPs from damaged lysosomes	Silica, cholesterol crystals, amyloid-β	32
6	Mitochondrial dysfunction	ROS production and mitochondrial damage promote NLRP3 activation	Oxidative stress, viral infections	33
7	ATP release and P2X7 activation	Extracellular ATP binds to the P2X7 receptor, triggering efflux of potassium ions	Cellular damage, inflammation	34
8	NEK7 interaction	NEK7 binds NLRP3 to promote its oligomerization	ROS, ion flux	5