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Area of Science:

  • Ophthalmology
  • Genetics
  • Cell Biology

Background:

  • Age-related macular degeneration (AMD) is a leading cause of blindness.
  • AMD involves retinal pigment epithelium (RPE) disorders and photoreceptor cell (PRC) death.
  • A strong genetic link exists between AMD and high-temperature requirement A 1 (HTRA1).

Purpose of the Study:

  • To investigate the role of HTRA1 in AMD pathogenesis.
  • To determine the relationship between HTRA1 expression and AMD phenotype.
  • To explore HTRA1 as a therapeutic target for AMD.

Main Methods:

  • Assessed HTRA1 expression in retinal cells from AMD-associated mutations and aging.
  • Utilized TUNEL assay and caspase analysis to confirm HTRA1-induced PRC death.
  • Generated transgenic zebrafish models overexpressing HTRA1 in PRCs and analyzed AMD-like features.
  • Investigated HTRA1 signaling pathways, including AKT-FOXO3 and TGF-β.
  • Tested the efficacy of HTRA1 inhibition using 6-boroV in zebrafish models.

Main Results:

  • HTRA1 expression is elevated in PRCs and RPE due to AMD mutations and aging.
  • Overexpression of HTRA1 in PRCs directly induces PRC death.
  • Zebrafish models with HTRA1 overexpression exhibited RPE changes, PRC death, and lipofuscin accumulation, resembling early AMD.
  • HTRA1 inhibition rescued PRC death in both AMD and retinitis pigmentosa zebrafish models.
  • AKT-FOXO3 signaling, activated by TGF-β, downstream of HTRA1, mediates PRC death.

Conclusions:

  • HTRA1 derived from PRCs contributes to early AMD through PRC death.
  • HTRA1 is implicated in the pathogenesis of AMD and other PRC degenerative diseases.
  • HTRA1 represents a promising therapeutic target for neuroprotective strategies in early AMD.