The therapeutic problem of proliferative diabetic retinopathy: Targeting somatostatin receptors

M. I. Davis, S. H. Wilson, M. B. Grant

Research output: Contribution to journalShort survey

43 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)295-299
Number of pages5
JournalHormone and Metabolic Research
Issue number5
StatePublished - Jul 7 2001


  • Angiogenesis
  • Apoptosis
  • Diabetic Retinopathy
  • Growth Hormone
  • Insulin-Like Growth Factor
  • Octreotide
  • Somatostatin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

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