Recent insights on modulation of inflammasomes by adipokines: a critical event for the pathogenesis of obesity and metabolism-associated diseases.

Aberrant production of adipokines, a group of adipocytes-derived hormones, is considered one of the most important pathological characteristics of obesity. In individuals with obesity, beneficial adipokines, such as adiponectin are downregulated, whereas leptin and other pro-inflammatory adipokines are highly upregulated. Hence, the imbalance in levels of these adipokines is thought to promote the development of obesity-linked complications. However, the mechanisms by which adipokines contribute to the pathogenesis of various diseases have not been clearly understood. Inflammasomes represent key signaling platform that triggers the inflammatory and immune responses through the processing of the interleukin family of pro-inflammatory cytokines in a caspase-1-dependent manner. Beyond their traditional function as a component of the innate immune system, inflammasomes have been recently integrated into the pathological process of multiple metabolism- and obesity-related disorders such as cardiovascular diseases, diabetes, fatty liver disease, and cancer. Interestingly, emerging evidence also highlights the role of adipokines in the modulation of inflammasomes activation, making it a promising mechanism underlying distinct biological actions of adipokines in diseases driven by inflammation and metabolic disorders. In this review, we summarize the effects of adipokines, in particular adiponectin, leptin, visfatin and apelin, on inflammasomes activation and their implications in the pathophysiology of obesity-linked complications.