title: Cardiovascular diabetology in the core of a novel interleukins classification: the bad, the good and the aloof.
abstract: BACKGROUND
  The impressive correlation between cardiovascular disease and glucose metabolism alterations has raised the likelihood that atherosclerosis and type 2 diabetes may share common antecedents. Inflammation is emerging as a conceivable etiologic mechanism for both. Interleukins are regulatory proteins with ability to accelerate or inhibit inflammatory processes.
  
  
  OBJECTIVE
  A novel interleukins classification is described, based on their role in diabetes and atherosclerosis, hypothesizing that each interleukin (IL) acts on both diseases in the same direction--regardless if harmful, favorable or neutral.
  
  
  METHODS
  The 29 known interleukins were clustered into three groups: noxious (the "bad", 8 members), comprising IL-1, IL-2, IL-6, IL-7, IL-8, IL-15, IL-17 and IL-18; protective (the "good", 5 members), comprising IL-4, IL-10, IL-11, IL-12 and IL-13; and "aloof", comprising IL-5, IL-9, IL-14, IL-16 and IL-19 through IL-29 (15 members). Each group presented converging effects on both diseases. IL-3 was reluctant to clustering.
  
  
  CONCLUSIONS
  These observations imply that 1) favorable effects of a given IL on either diabetes or atherosclerosis predicts similar effects on the other; 2) equally, harmful IL effects on one disease can be extrapolated to the other; and 3) absence of influence of a given IL on one of these diseases forecasts lack of effects on the other. These facts further support the unifying etiologic theory of both ailments, emphasizing the importance of a cardiovascular diabetologic approach to interleukins for future research. Pharmacologic targeting of these cytokines might provide an effective means to simultaneously control both atherosclerosis and diabetes.
authors.affiliation: Cardiac Rehabilitation Institute, Sheba Medical Center, 52621 Tel-Hashomer, Israel. zfisman@post.tau.ac.il
authors.forename: Enrique Z
authors.initials: EZ
authors.lastname: Fisman
authors.forename: Michael
authors.initials: M
authors.lastname: Motro
authors.forename: Alexander
authors.initials: A
authors.lastname: Tenenbaum