Neuroprotective Strategy in Retinal Degeneration: Suppressing ER Stress-Induced Cell Death via Inhibition of the mTOR Signal

Int J Mol Sci. 2017 Jan 19;18(1):201. doi: 10.3390/ijms18010201.

Abstract

The retina is a specialized sensory organ, which is essential for light detection and visual formation in the human eye. Inherited retinal degenerations are a heterogeneous group of eye diseases that can eventually cause permanent vision loss. UPR (unfolded protein response) and ER (endoplasmic reticulum) stress plays an important role in the pathological mechanism of retinal degenerative diseases. mTOR (the mammalian target of rapamycin) kinase, as a signaling hub, controls many cellular processes, covering protein synthesis, RNA translation, ER stress, and apoptosis. Here, the hypothesis that inhibition of mTOR signaling suppresses ER stress-induced cell death in retinal degenerative disorders is discussed. This review surveys knowledge of the influence of mTOR signaling on ER stress arising from misfolded proteins and genetic mutations in retinal degenerative diseases and highlights potential neuroprotective strategies for treatment and therapeutic implications.

Keywords: ER stress; apoptosis; mTOR; retinal degeneration; retinal neuroprotection; unfolded protein response.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Death / drug effects
  • Endoplasmic Reticulum Stress* / drug effects
  • Humans
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use*
  • Retinal Degeneration / drug therapy*
  • Retinal Degeneration / pathology*
  • Signal Transduction* / drug effects
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Neuroprotective Agents
  • TOR Serine-Threonine Kinases