Roles of Calcium and Tyrosine Kinases in the Pathogenesis of Type 2 Diabetes Mellitus

J.   A.   Rosado; P.   C.   Redondo; J.   A.   Pariente; G.   M.   Salido

doi:10.2174/157340806775473553

Abstract

Diabetes mellitus type 2 is a metabolic disease associated with chronic hyperglycaemia, which leads to a wide range of complications, including microvascular and macrovascular alterations, retinopathy, nephropathy and renal disease or peripheral neuropathy. Several intracellular pathways have been shown to be associated to type 2 diabetes mellitus, ranging from an altered insulin receptor-associated signalling to an abnormal intracellular calcium homeostasis or disturbances in Na+ handling. A number of diabetes-associated complications have been reported to be associated with hyperactivity of certain protein tyrosine kinases, such as those cytosolic kinases of the Src family, involved in the altered intracellular calcium mobilisation and platelet-derived cardiovascular problems and in glomerular injury, or the JAK family of tyrosine kinases involved in hyperglycaemia-induced renal failure. There has been a considerable effort in several laboratories to identify suitable targets for the design of drugs against this disease. The development of tyrosine kinase inhibitors suitable for medical purposes might represent a significant advance in the therapy of complications associated to type 2 diabetes mellitus.

Keywords: Type 2 diabetes mellitus, calcium homeostasis, tyrosine kinases

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