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 infectious/
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 interferoninducible
nuclear antigens). After activation by PAMPs or DAMPs, NLRP3 inflammasome promotes conversion of procaspase
1 in caspase-1 to form the active complex which is able to cleave pro-IL-1β and pro-IL-18 in respective active inflammatory
cytokines IL-1β 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 their
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.