Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies
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.
Authors
- Kaiyan Yu (ORCID: https://orcid.org/0000-0001-5962-8968)
- Xiangyu Chen (ORCID: https://orcid.org/0000-0001-7947-3211)
- Juan Zhang (ORCID: https://orcid.org/0000-0003-4673-3448)
- Zhenyu Wu (ORCID: https://orcid.org/0000-0003-4478-0734)
- Hongjie Di
Institutions
- Nanjing University of Chinese Medicine (CN)
Publication Details
- Journal
- International Journal of Molecular Sciences
- Published
- 2026-05-27
- DOI
- https://doi.org/10.3390/ijms27114819
- Primary Topic
- Inflammasome and immune disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00