Review highlights mitochondrial mechanisms driving NLRP3 inflammasome in diabetic kidney disease, suggesting therapeutic targets.
Despite current therapies, persistent chronic inflammation remains an important contributor to residual renal risk in diabetic kidney disease (DKD). The NLRP3 inflammasome is a key driver of this inflammatory cascade, with mitochondria serving as a central hub that translates metabolic stress into NLRP3 activation via mitochondrial reactive oxygen species (mtROS) and oxidized mitochondrial DNA (ox-mtDNA). This review delineates the signaling network of the mitochondria–NLRP3 inflammasome axis in DKD and evaluates its potential as a therapeutic target to improve patient outcomes.
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Chen et al. (2026) studied this question.
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