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Cardiovascular Diabetology: Clinical, Metabolic and Inflammatory Facets

Editor(s): Fisman E.Z. (Holon) 
Tenenbaum A. (Tel-Hashomer) 
Table of Contents
Vol. 45, No. , 2008
Section title: Paper
Fisman EZ, Tenenbaum A (eds): Cardiovascular Diabetology: Clinical, Metabolic and Inflammatory Facets. Adv Cardiol. Basel, Karger, 2008, vol 45, pp 44-64
(DOI:10.1159/000115187)

Biomarkers in Cardiovascular Diabetology: Interleukins and Matrixins

Fisman E. · Adler Y. · Tenenbaum A.
aCardiovascular Diabetology Research Foundation, Holon, b Cardiac Rehabilitation Institute, Chaim Sheba Medical Center, Tel-Hashomer, affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel

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Abstract

The impressive correlation between cardiovascular disease and alterations in glucose metabolism 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, and matrixins are prepro enzymes responsible for the timely breakdown of extracellular matrix. Interleukins (ILs) are classified based on their role in diabetes and atherosclerosis, hypothesizing that each interleukin acts on both diseases in the same direction - regardless if harmful, favorable or neutral. They are 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 and IL-30 through 33 were not included due to the scarce available data. It may be seen that (1) favorable effects of a given interleukin on either diabetes or atherosclerosis predicts similar effects on the other; (2) equally, harmful interleukin effects on one disease can be extrapolated to the other, and (3) absence of influence of a given interleukin on one of these diseases forecasts lack of effects on the other. Matrixins seem to present a similar pathophysiological pattern. These facts further support the unifying etiologic theory of diabetes and heart disease, emphasizing the importance of a cardiovascular diabetologic approach to these cytokines for future research. A pharmacologic simultaneous targeting of interleukins and matrixins might provide an effective means to concurrently control both atherosclerosis and diabetes.



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