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The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications
Kai Ding1, Chao Song2,3, Hengjing Hu1,3,4
1Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan Province 421001, China.
Insights
Diabetic cardiomyopathy (DCM) involves the NLRP3 inflammasome, a key immune pathway. Targeting this inflammasome offers potential new treatments for DCM, a complication of diabetes mellitus (DM).
Area of Science:
- Immunology
- Cardiology
- Endocrinology
Background:
- Diabetic cardiomyopathy (DCM) is a severe complication of diabetes mellitus (DM) with unclear molecular mechanisms.
- The nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome is crucial for innate immunity.
- Dysregulated NLRP3 inflammasome activation leads to cytokine overproduction and pyroptosis, contributing to inflammatory diseases.
Purpose of the Study:
- To summarize the cell-specific role of the NLRP3 inflammasome in DCM.
- To provide insights into developing therapeutic strategies targeting the NLRP3 inflammasome for DCM.
Main Methods:
- This narrative review synthesizes existing research on NLRP3 inflammasome involvement in DCM.
- It examines studies indicating the participation of NLRP3 inflammasome activation in DCM development and progression.
Main Results:
- Evidence suggests NLRP3 inflammasome activation plays a role in the pathogenesis of DCM.
- Interventions targeting the NLRP3 inflammasome have shown potential in mitigating DCM progression.
Conclusions:
- The NLRP3 inflammasome is implicated in DCM development.
- Targeting the NLRP3 inflammasome presents a promising therapeutic avenue for managing diabetic cardiomyopathy.
Abstract:
Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus (DM). However, the precise molecular mechanisms remain largely unclear, and it is still a challenging disease to diagnose and treat. The nucleotide-binding oligomerization domain and leucine-rich repeat pyrin 3 domain (NLRP3) inflammasome is a critical part of the innate immune system in the host to defend against endogenous danger and pathogenic microbial infections. Dysregulated NLRP3 inflammasome activation results in the overproduction of cytokines, primarily IL-1β and IL-18, and eventually, inflammatory cell death-pyroptosis. A series of studies have indicated that NLRP3 inflammasome activation participates in the development of DCM, and that corresponding interventions could mitigate disease progression. Accordingly, this narrative review is aimed at briefly summarizing the cell-specific role of the NLRP3 inflammasome in DCM and provides novel insights into developing DCM therapeutic strategies targeting the NLRP3 inflammasome.
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