Metainflammation in Diabetic Coronary Artery Disease: Emerging Role of Innate and Adaptive Immune Responses

被引:29
|
作者
Aravindhan, Vivekanandhan [1 ]
Madhumitha, Haridoss [2 ]
机构
[1] Univ Madras, Dr ALM PG IBMS, Dept Genet, Chennai 600113, Tamil Nadu, India
[2] Anna Univ, AU KBC Res Ctr, MIT Campus, Chennai 600044, Tamil Nadu, India
关键词
TOLL-LIKE RECEPTORS; PRO-INFLAMMATORY CYTOKINE; SMOOTH-MUSCLE CELLS; NOD-LIKE RECEPTORS; INSULIN-RESISTANCE; DENDRITIC CELLS; METABOLIC ENDOTOXEMIA; NEGATIVE REGULATION; SKELETAL-MUSCLE; BETA LEVELS;
D O I
10.1155/2016/6264149
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Globally, noncommunicable chronic diseases such as Type-2 Diabetes Mellitus (T2DM) and Coronary Artery Disease (CAD) are posing a major threat to the world. T2DM is known to potentiate CAD which had led to the coining of a new clinical entity named diabetic CAD (DM-CAD), leading to excessive morbidity and mortality. The synergistic interaction between these two comorbidities is through sterile inflammation which is now being addressed as metabolic inflammation or metainflammation, which plays a pivotal role during both early and late stages of T2DM and also serves as a link between T2DM and CAD. This review summarises the current concepts on the role played by both innate and adaptive immune responses in setting up metainflammation in DM-CAD. More specifically, the role played by innate pattern recognition receptors (PRRs) like Toll-like receptors (TLRs), NOD1-like receptors (NLRs), Rig-1-like receptors (RLRs), and C-type lectin like receptors (CLRs) and metabolic endotoxemia in fuelling metainflammation in DM-CAD would be discussed. Further, the role played by adaptive immune cells (Th1, Th2, Th17, and Th9 cells) in fuelling metainflammation in DM-CAD will also be discussed.
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页数:10
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