Neuropeptides, trophic factors, and other substances providing morphofunctional and metabolic protection in experimental models of diabetic retinopathy

Int Rev Cell Mol Biol. 2014;311:1-121. doi: 10.1016/B978-0-12-800179-0.00001-5.

Abstract

Vision is the most important sensory modality for many species, including humans. Damage to the retina results in vision loss or even blindness. One of the most serious complications of diabetes, a disease that has seen a worldwide increase in prevalence, is diabetic retinopathy. This condition stems from consequences of pathological metabolism and develops in 75% of patients with type 1 and 50% with type 2 diabetes. The development of novel protective drugs is essential. In this review we provide a description of the disease and conclude that type 1 diabetes and type 2 diabetes lead to the same retinopathy. We evaluate existing experimental models and recent developments in finding effective compounds against this disorder. In our opinion, the best models are the long-term streptozotocin-induced diabetes and Otsuka Long-Evans Tokushima Fatty and spontaneously diabetic Torii rats, while the most promising substances are topically administered somatostatin and pigment epithelium-derived factor analogs, antivasculogenic substances, and systemic antioxidants. Future drug development should focus on these.

Keywords: Antiapoptotic pathways; Müller glia; Retinal neurons; Retinal pigment epithelium; Retinal vasculature; Retinoprotection; Visual functions.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Diabetic Retinopathy / epidemiology
  • Diabetic Retinopathy / metabolism*
  • Diabetic Retinopathy / pathology*
  • Diabetic Retinopathy / therapy
  • Disease Models, Animal
  • Humans
  • Nerve Growth Factors / metabolism*
  • Neuropeptides / metabolism*
  • Prevalence

Substances

  • Nerve Growth Factors
  • Neuropeptides