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Diabetes and Vascular Disease Research
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Protein kinase C β inhibition: a novel therapeutic strategy for diabetic microangiopathy

Iskandar Idris

John Peace Diabetes Centre, Kings Mill Hospital, Sherwood Forest Hospitals NHS Trust, Mansfield Road, Nottinghamshire, UK

Richard Donnelly

University of Nottingham, Derby Hospitals NHS Foundation Trust, UK

Biochemical mechanisms involved in hyperglycaemia-induced vascular damage include alterations in cellular signalling by activation of protein kinase C (PKC). Twelve isoforms of PKC have been characterised according to their structure and co-factor requirements. Activation of PKC is mediated primarily through increased release of diacylglycerol (DAG). Adverse effects of PKC and DAG on vascular function include increased permeability, endothelial cell activation, altered blood flow, leukocyte adhesion and abnormal growth factor signalling.

A highly selective and orally active PKC-β isoform-selective inhibitor, ruboxistaurin, has been developed. Initial studies suggest that this agent decreased the development of sight-threatening macular oedema and the occurrence of visual loss. It did not, however, prevent the progression of diabetic retinopathy.

Key Words: diabetes • vascular function • retinopathy • protein kinase C • ruboxistaurin

Diabetes and Vascular Disease Research, Vol. 3, No. 3, 172-178 (2006)
DOI: 10.3132/dvdr.2006.026
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