Three Major Causes of Metabolic Retinal Degenerations and Three Ways to Avoid Them

Int J Mol Sci. 2023 May 13;24(10):8728. doi: 10.3390/ijms24108728.

Abstract

An imbalance of homeostasis in the retina leads to neuron loss and this eventually results in a deterioration of vision. If the stress threshold is exceeded, different protective/survival mechanisms are activated. Numerous key molecular actors contribute to prevalent metabolically induced retinal diseases-the three major challenges are age-related alterations, diabetic retinopathy and glaucoma. These diseases have complex dysregulation of glucose-, lipid-, amino acid or purine metabolism. In this review, we summarize current knowledge on possible ways of preventing or circumventing retinal degeneration by available methods. We intend to provide a unified background, common prevention and treatment rationale for these disorders and identify the mechanisms through which these actions protect the retina. We suggest a role for herbal medicines, internal neuroprotective substances and synthetic drugs targeting four processes: parainflammation and/or glial cell activation, ischemia and related reactive oxygen species and vascular endothelial growth factor accumulation, apoptosis and/or autophagy of nerve cells and an elevation of ocular perfusion pressure and/or intraocular pressure. We conclude that in order to achieve substantial preventive or therapeutic effects, at least two of the mentioned pathways should be targeted synergistically. A repositioning of some drugs is considered to use them for the cure of the other related conditions.

Keywords: Müller glia; anti-apoptotic pathways; plant extracts; protective factors; retinal neurons; retinal pigment epithelium; retinal vasculature; retinoprotection; visual functions.

Publication types

  • Review

MeSH terms

  • Diabetic Retinopathy* / metabolism
  • Glaucoma* / metabolism
  • Humans
  • Retina / metabolism
  • Retinal Degeneration* / etiology
  • Retinal Degeneration* / metabolism
  • Retinal Degeneration* / prevention & control
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Vascular Endothelial Growth Factor A