Background: Inflammation is an innate immune response which is considered a common basis for several diseases such as ageing, diabetes, obesity, gout, neurodegenerative diseases and others. Among other platforms, inflammasomes are part of a superfamily of Pattern Recognition Receptors (PRR) and act as cytoplasmatic sensors for stimulation with Pathogen Associated Molecular Pattern (PAMPs) and/or Danger/Damage-Associated Molecular Patterns (DAMPs) leading to an infec-tious/pathogenic or sterile inflammation. Inflammasomes constitute a complex platform with high molecular weight and functionality, divided into two families: NOD-like or NLR and PYHIN (pyrin and HIN200 - hematopoietic interferon-inducible nuclear antigens). After activation by PAMPs or DAMPs, NLRP3 inflammasome promotes conversion of pro-caspase 1 in caspase-1 to form the active complex which is able to cleave pro-IL-ip and pro-IL-18 in respective active inflammatory cytokines IL-ip and IL-18 inducing cellular death by pyroptosis. Diabetes has a very intricate pathology with metabolic adaptation and inflammatory components apparently responsible for diabetic complications. Objective: The present review evaluates the role of inflammasome, emphasizing NRLP3 on diabetes. An overview on several inflammatory diseases in which inflammasomes appear to play a role is included. Patents on inflammasomes associated with diabetes are evaluated and discussed. Conclusion: There are a significant number of patents on inflammation but few of them are specifically on inflammasome and diabetes. The patents WO2015003246; US20130273588; WO2012016145; and CN104258398 are shown and then-mechanisms are discussed. In conclusion, deeply studies on inflammasomes mechanisms will help the proposition of new therapeutic targets for controlling inflammatory process in diabetic complications.
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