Horm Metab Res 2001; 33(5): 295-299
DOI: 10.1055/s-2001-15286
Mini-Review

© Georg Thieme Verlag Stuttgart · New York

The Therapeutic Problem of Proliferative Diabetic Retinopathy: Targeting Somatostatin Receptors

M. I.  Davis, S. H.  Wilson, M. B.  Grant
  • Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, FL, USA
Further Information

Publication History

Publication Date:
31 December 2001 (online)

Clinical management of proliferative diabetic retinopathy has changed very little in the last 5 decades, relying primarily on laser ablation of the retinal vasculature. Several lines of clinical and experimental evidence suggest that somatostatin analogues may be efficacious in inhibiting neovascularization associated with proliferative retinopathy but the mechanism of action for these compounds is unclear. Inhibition of growth hormone secretion and the subsequent suppression of insulin-like growth factor 1 (IGF-1) production by somatostatin has been suggested as the mechanism of action, however, in vitro studies suggest that somatostatin analogues suppress endothelial cell growth through a direct, somatostatin receptor-mediated inhibition of pro-survival signaling pathways. The advent of a new generation of modified peptide and peptidomimetic somatostatin analogues has allowed investigators to more carefully define the receptor subtypes responsible for somatostatin-induced endothelial cell death and may eventually lead to the clinical development of somatostatin analogues that can reduce endothelial cell proliferation, independent of suppression of circulating hormone levels.

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M. B. Grant

Department of Pharmacology and Therapeutics
University of Florida College of Medicine

P. O. Box 100267
Gainesville, Fl 32610
USA


Email: E-mail:grantma@pharmacology.ufl.edu

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