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Immunoinflammatory and Insulinomimetic Modulators of Cell Signaling: Approach to Diabetes Therapy

Call for Papers

Emerging experimental and clinical studies suggest a significant role for immunoinflammatory mediators in the development of diabetes mellitus and its complications. Inflammation plays a pivotal role in the pathogenesis of both forms of diabetes and manifests in a variety of cells ranging from pancreatic β-cells to immune cells. Various infective, stress, or danger signals may be responsible for the persistent inflammation observed in diabetes. The studies providing a link between activation of immune response and specific genetic predisposition could lead to development of effective therapies and better screening of predisposed individuals. Furthermore, targeting the specific components of the immunoinflammatory cascade may aid the development of new therapies for prevention of diabetic complications.

The main focus of this special issue would be to explore the biological crosstalk between immunoinflammatory and insulinomimetic modulators representing T2DM and T1DM therapies. Among experimental insulin mimetic substances, the focus will be on pharmacological effects of newly synthesized chemicals or drugs and substances extracted from natural plants, capable of affecting insulin release, insulin signaling, or inflammation. In addition, new reports on the effects of dipeptidyl-peptidase (DPP-4) inhibition in T1DM and T2DM will be considered. These studies may be at the level of genetic and epigenetic factors, signal transduction pathway, and the activated immune response affecting insulin secretion, β-cell destruction, insulin signaling, or peripheral insulin resistance. Other potential reports may consist of possible innate immunity, inflammatory, and glyco-oxidative stress responses modulators that may delay the development of diabetes and its complications.

The topics to be covered by this special issue may provide an avenue for new effective therapies for preventing diabetes and its complications by modulating the crucial pathophysiological and biochemical defects. Potential topics include, but are not limited to:

  • New experimental diabetes models delineating insulin and immune cell signaling
  • Oxidative and nitrosative stress modulators in preventing the development of diabetes and its complications
  • Mechanisms of β-cell destruction: role of mitochondrial and EPR stress
  • Role of innate/adaptive immunity and inflammation in the pathogenesis of diabetes and its complications
  • New therapeutic modulators of immune cell function and inflammation in diabetes
  • Therapeutic potential of new DPP-4/CD26 inhibitors in diabetes treatment
  • Novel glucose lowering and insulin sensitizing drugs: chemicals, enzyme inhibitors, hormones, neuromediators, amino acids and plant based purified products
  • Genetics and diabetes: predisposition, gene polymorphisms, and epigenetic changes

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/jdr/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/jdr/iics/ according to the following timetable:

Manuscript DueFriday, 5 April 2013
First Round of ReviewsFriday, 28 June 2013
Publication DateFriday, 23 August 2013

Lead Guest Editor

  • Gordana Kocic, Medical Faculty University Nis, Bul Dr Zorana Djindjica 81, 18000 Nis, Serbia

Guest Editors

  • Mohan R. Dasu, Department of Dermatology, University of California at Davis 3301, CA 95816, USA
  • Norihide Yokoi, Division of Cellular and Molecular Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe 650-0047, Japan