Citation
Subramaniam, Shamala Devi and Abas, Razif
(2025)
The role of the NLRP3 inflammasome in Type 1 Diabetes: insights from a systematic literature review of rodent studies.
Malaysian Journal of Medicine and Health Sciences, 21 (3).
pp. 457-464.
ISSN 1675-8544; eISSN: 2636-9346
Abstract
Introduction: Type 1 Diabetes mellitus (T1DM) is an autoimmune disease characterized by the destruction of pancreatic β-cells, necessitating lifelong insulin therapy. The rising incidence of T1DM imposes a significant economic burden worldwide, particularly in countries like Malaysia with high diabetes rates. The NLRP3 inflammasome, crucial for regulating inflammation, has emerged as a potential therapeutic target for T1DM due to its involvement in immune dysfunction and tissue damage. This study reviews existing literature and experimental data to clarify the NLRP3 inflammasome's role in T1DM development and progression. Materials and methods: We conducted a systematic search across five electronic databases (Scopus, Science Direct, Sage Journals, Wiley Online Library, and SpringerLink) from 2000 to 2024 using keywords such as "NLRP3," "inflammasome," "rat," "rabbit," and "mice." Data were extracted using a predefined Excel template, covering study objectives, rodent models, NLRP3 inflammasome treatment, findings, and limitations. A systematic review approach was used to analyze and synthesize the results-Results: The review highlights a consistent upregulation of NLRP3 inflammasome activity in T1DM, suggesting its role in disease pathophysiology. Studies on NLRP3 inhibitor compound (MCC950), showed promising results in reducing neurovascular remodeling, improving cognitive function, and enhancing survival rates post-stroke in diabetic animals. Additionally, NLRP3 inhibition facilitated alveolar bone healing in diabetic rats, indicating its potential in tissue repair and regeneration. Conclusion: Targeting the NLRP3 inflammasome offers a promising strategy for managing T1DM. However, further research is needed to understand its mechanisms fully and to develop therapeutic strategies that improve patient outcomes and address T1DM-related complications.
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