Generic placeholder image

Current Neuropharmacology

Editor-in-Chief

ISSN (Print): 1570-159X
ISSN (Online): 1875-6190

Review Article

Growth Factors in the Pathogenesis of Retinal Neurodegeneration in Diabetes Mellitus

Author(s): Ben-Skowronek Iwona

Volume 14, Issue 8, 2016

Page: [792 - 804] Pages: 13

DOI: 10.2174/1570159X14666160813182009

Price: $65

Abstract

Neurodegeneration is an initial process in the development of diabetic retinopathy (DR).

High quantities of glutamate, oxidative stress, induction of the renin-angiotensin system (RAS) and elevated levels of RAGE are crucial elements in the retinal neurodegeneration caused by diabetes mellitus. At least, there is emerging proof to indicate that the equilibrium between the neurotoxic and neuroprotective components will affect the state of the retinal neurons.

Somatostatin (SST), pigment epithelium-derived factor (PEDF), and erythropoietin (Epo) are endogenous neuroprotective peptides that are decreased in the eye of diabetic persons and play an essential role in retinal homeostasis. On the other hand, insulin-like growth factor 1 (IGF-1), and vascular endothelial growth factor (VEGF) are pivotal proteins which participate in the development of new capillaries and finally cause damage to the retinal neurons. During recent years, our knowledge about the function of growth factors in the pathogenesis of retinal neurodegeneration has increased. However, intensive investigations are needed to clarify the basic processes that contribute to retinal neurodegeneration and its association with damage to the capillary blood vessels. The objective of this review article is to show new insights on the role of neurotransmitters and growth factors in the pathogenesis of diabetic retinopathy. The information contained in this manuscript may provide the basis for novel strategies based on the factors of neurodegeneration to diagnose, prevent and treat DR in its earliest phases.

Keywords: Diabetic retinopathy, growth factors, neurotransmitter, retinal neurodegeneration.

Graphical Abstract

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy