The NLRP3 inflammasome in chronic kidney disease progression: systematic review of preclinical models reveals a critical gap in pyroptosis research and therapeutic translation.

The NOD-like receptor protein 3 (NLRP3) inflammasome has emerged as a central regulator of inflammatory, fibrotic, and mitochondrial injury during chronic kidney disease pathogenesis.

We found that across all model types, NLRP3 activation was consistently associated with upregulated caspase-1, elevated IL-1β and IL-18, and a decline in renal function, tubular injury, interstitial fibrosis, and mitochondrial dysfunction.