Abstract
Metabolic syndrome (MS) is a serious health problem worldwide; it is characterized by a group of metabolic disorders, including central obesity, insulin resistance/type 2 diabetes, hyperlipidemia with accelerated atherosclerosis, hypertension, non-alcoholic fatty liver disease, and elevated uric acid with increased risk of gout. The incidence of MS has increased considerably in recent decades and has attracted considerable attention. A number of clinical and translational laboratory studies have implicated the activation of nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome in the development of MS, therefore establishing a strong link between chronic inflammation and metabolic diseases. This paper aims to review new developments on NLRP3 inflammasome in MS for better understanding of chronic inflammation in metabolic diseases. We will also provide new insights into using NLRP3 inflammasome as an innovative therapeutic target.
Highlights
Accumulating evidence strongly links chronic inflammation to metabolic syndrome (MS)
Consistent with in vitro studies, atherosclerotic-prone low-density lipoprotein (LDL)-receptor-deficient mice that were reconstituted with bone marrow from nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3)-/, ASC-/, or IL-1β-/mice developed many fewer atherosclerotic plaques and less aortic lesion size than those reconstituted with wildtype bone marrow (Egan, et al, 2011). All these findings suggest that NLRP3 inflammasome activation is a key event in atherosclerosis
The activation of NLRP3 inflammasome, which contributes to pathophysiological mechanisms that explain MS development, is beginning to be characterized in detail
Summary
Accumulating evidence strongly links chronic inflammation to metabolic syndrome (MS). A number of recent landmark studies have demonstrated that chronic inflammation is the key feature and basis of MS (Hotamisligil, 2006; Fève and Bastard, 2009). A wide variety of immune cells, such as macrophages, monocytes, and T cells, have been shown to infiltrate the adipose tissue, liver, and pancreatic islets in the development of MS (Stienstra et al, 2012). Numerous pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukins (ILs), and adipokines which are secreted by adipocytes, participate in the pathogenesis of MS. Interest has been focused on the role of a multiprotein complex called nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome, which controls the processing and.
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