Co-targeting of glial activation and inflammation by tsRNA-Gln-i-0095 for treating retinal ischemic pathologies

Cell Commun Signal. 2025 Jan 10;23(1):18. doi: 10.1186/s12964-024-02013-x.

Abstract

Ischemic retinopathies are the major causes of blindness, yet effective early-stage treatments remain limited due to an incomplete understanding of the underlying molecular mechanisms. Significant changes in gene expression often precede structural and functional alterations. Transfer RNA (tRNA)-derived small RNAs (tsRNAs) are emerging as novel gene regulators, involved in various biological processes and human diseases. In this study, tsRNA-Gln-i-0095 was identified as a novel regulator, which was significantly upregulated in retinal ischemia/reperfusion (I/R) injury. Reducing the levels of tsRNA-Gln-i-0095 suppressed reactive gliosis, lowered inflammatory cytokine levels, and protected retinal ganglion cells from I/R injury. These effects led to reduced structural and functional damage, inhibited glial activation and inflammation, and enhanced neuronal function. Mechanistically, tsRNA-Gln-i-0095 downregulated the expression of NFIA and TGFBR2 through a miRNA-like mechanism. Collectively, this study highlights the potential of targeting tsRNA-Gln-i-0095 as a novel therapeutic approach to reduce retinal I/R injury and preserve visual function.

Keywords: Ischemic/reperfusion injury; Müller cells; Reactive gliosis; Retinal ganglion cells; tsRNA.

MeSH terms

  • Animals
  • Humans
  • Inflammation* / genetics
  • Inflammation* / metabolism
  • Inflammation* / pathology
  • Ischemia / metabolism
  • Ischemia / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Neuroglia* / metabolism
  • Neuroglia* / pathology
  • RNA, Transfer / genetics
  • RNA, Transfer / metabolism
  • Reperfusion Injury* / genetics
  • Reperfusion Injury* / metabolism
  • Reperfusion Injury* / pathology
  • Retina / metabolism
  • Retina / pathology
  • Retinal Diseases / genetics
  • Retinal Diseases / metabolism
  • Retinal Diseases / pathology
  • Retinal Ganglion Cells / metabolism
  • Retinal Ganglion Cells / pathology

Substances

  • RNA, Transfer
  • MicroRNAs