Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to sign up for SAGE Journal Email Alerts today!

Sign In to gain access to subscriptions and/or personal tools.
Diabetes and Vascular Disease Research
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Idris, I.
Right arrow Articles by Donnelly, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Idris, I.
Right arrow Articles by Donnelly, R.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

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
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
M. Matz, U. Weber, M.-F. Mashreghi, C. Lorkowski, J. Ladhoff, S. Kramer, H.-H. Neumayer, and K. Budde
Effects of the new immunosuppressive agent AEB071 on human immune cells
Nephrol. Dial. Transplant., January 25, 2010; (2010): gfp775v1 - gfp775.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
N. B. Bishara and H. Ding
Glucose enhances expression of TRPC1 and calcium entry in endothelial cells
Am J Physiol Heart Circ Physiol, January 1, 2010; 298(1): H171 - H178.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
E. N. Lavrentyev and K. U. Malik
High glucose-induced Nox1-derived superoxides downregulate PKC-{beta}II, which subsequently decreases ACE2 expression and ANG(1-7) formation in rat VSMCs
Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H106 - H118.
[Abstract] [Full Text] [PDF]