Background: The intracellular multiprotein complex termed the inflammasome functions
as a platform of pro-inflammatory cytokine production such as IL-1β and IL-18. Under certain conditions,
however, the inflammasome produces non-canonical effects such as induction of cell death, pyroptosis
and cell metabolism alterations.
Objective: In mammalian cells, several types of inflammasomes were identified, but the most widely
studied one is the inflammasome containing NOD-like receptor with pyrin domain 3 (NLRP3), which
has recently been reported as a central pathogenic mechanism of chronic degenerative diseases. Many
activators or risk factors exert their actions through the activation of the NLRP3 inflammasome to
produce a variety of functional changes in different cells including inflammatory, metabolic or survival
responses. Several molecular signaling pathways are shown to mediate the activation of the
NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome
leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production. In the
kidney, inflammation is believed to mediate or promote the progression of glomerular sclerotic pathologies
resulting in end-stage renal disease (ESRD). NLRP3 inflammasome activation may turn on
glomerular inflammation and other cell damages, contributing to the onset of glomerular injury and
ESRD. This inflammasome activation not only occurs in immune cells, but also in residential cells
such as endothelial cells and podocytes in the glomeruli.
Summary: This review briefly summarizes current evidence of NLRP3 inflammasome activation and
related molecular mechanisms in renal glomeruli. The possible canonical and non-canonical effects of
this inflammasome activation and its potential implication in the development of different glomerular
diseases are highlighted.