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Inflammasomes and type 2 diabetes: An updated systematic review
Zahra Sepehri1, Zohre Kiani2, Mahdi Afshari3
1Department of Internal Medicine, Zabol University of Medical Sciences, Zabol, Iran.
Immunology Letters
|October 29, 2017
Summary
Inflammasomes, key sensors of cellular stress, are implicated in type 2 diabetes (T2D) inflammation. This review explores their role in T2D pathogenesis and complications.
Area of Science:
- Immunology
- Metabolic Disorders
- Molecular Biology
Background:
- Type 2 diabetes (T2D) is characterized by chronic inflammation.
- The precise mechanisms driving inflammation in T2D remain unclear.
- Intracellular sensors recognizing damage-associated molecular patterns (DAMPs) are suspected to be involved.
Purpose of the Study:
- To systematically review the current understanding of inflammasome roles in T2D pathogenesis.
- To evaluate the contribution of inflammasomes to T2D complications.
Main Methods:
- Systematic literature review.
- Analysis of studies investigating inflammasomes (NLRP1, NLRP3) and their signaling pathways (caspase-1, IL-1β, IL-18).
Main Results:
- NLRP family inflammasomes are crucial intracellular receptors for inflammatory triggers.
- NLRP1 and NLRP3 inflammasomes are implicated in internal immunity, inflammation, and metabolic disorders.
- These inflammasomes may drive chronic inflammation in T2D patients.
Conclusions:
- Inflammasomes play a significant role in the inflammatory processes underlying T2D.
- Understanding inflammasome involvement is critical for T2D pathogenesis and complication research.
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