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Hif1a and Hif2a can be safely inactivated in cone photoreceptors

Marijana Samardzija1, Maya Barben2, Vyara Todorova2

  • 1Lab for Retinal Cell Biology, Department of Ophthalmology, University of Zurich, Schlieren, CH-8952, Switzerland. marijana.samardzija@usz.uzh.ch.

Scientific Reports
|November 8, 2019
PubMed

Insights

Hypoxia-inducible factors (HIFs) are implicated in age-related macular degeneration (AMD). Ablating HIFs in cone photoreceptors did not harm retinal function or survival, suggesting potential safety for anti-HIF therapies in AMD treatment.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Impaired tissue oxygenation causes hypoxia, activating hypoxia-inducible transcription factors (HIFs).
  • Chronic HIF activation is a potential factor in age-related macular degeneration (AMD) etiology.
  • HIF1 and HIF2 are emerging therapeutic targets for AMD.

Purpose of the Study:

  • To evaluate the consequences of anti-HIF therapies on retinal physiology and function.
  • To assess the role of HIFs in cone photoreceptors for potential AMD treatments.

Main Methods:

  • Generated mouse lines with Hif1a or both Hif1a and Hif2a ablated specifically in cone photoreceptors.
  • Assessed pathological alterations, retinal function, and hypoxic tolerance in these mouse lines.

Main Results:

  • HIF ablation in cone photoreceptors did not cause photoreceptor loss, retinal degeneration, or vascular abnormalities.
  • Retinal function remained unaffected, and hypoxic tolerance was similar to control mice.
  • HIF transcription factors are dispensable for normal cone function and survival in adult mouse retinas.

Conclusions:

  • HIFs are not essential for maintaining cone photoreceptor function and survival in adult mice.
  • This study provides foundational safety data for anti-HIF therapies targeting cone photoreceptors.
  • These findings support strategies for treating hypoxic retinal degenerative diseases like AMD by antagonizing HIF1A and HIF2A.

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