title: Inflammasome as a New Therapeutic Target for Diabetic Complications.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.forename: Caroline M O
authors.initials: CM
authors.lastname: Volpe
authors.forename: Paula M F
authors.initials: PM
authors.lastname: Anjos
authors.affiliation: Núcleo de Pós Graduação e Pesquisa (NPGP), Hospital Santa Casa de Misericórdia de Belo Horizonte - Belo Horizonte - MG, Brazil. nogueira.machado@pq.cnpq.br.
authors.forename: José A
authors.initials: JA
authors.lastname: Nogueira-Machado
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D048909:Diabetes Complications / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D003920:Diabetes Mellitus / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D055808:Drug Discovery; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007113:Immunity, Innate / Q000187:drug effects; D058847:Inflammasomes / Q000037:antagonists & inhibitors* / Q000378:metabolism; D058990:Molecular Targeted Therapy; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000037:antagonists & inhibitors / Q000378:metabolism; D010330:Patents as Topic; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000893:Anti-Inflammatory Agents; D007004:Hypoglycemic Agents; D058847:Inflammasomes; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human