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Ythdf2 loss in microglia aggravates ischemic retinopathy by increasing microglia activation and microvascular

Hong-Jing Zhu1, Yi-Chen Zhang2, Ye-Ran Zhang2

  • 1Department of Ophthalmology, The First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing 210029, China; Department of Ophthalmology, Children's Hospital of Nanjing Medical University, Nanjing 210029, China.

Journal of Advanced Research
|February 2, 2026
PubMed
Abstract

Insights

Loss of YTHDF2 in microglia disrupts retinal blood vessel development and worsens disease by affecting ACE and BMP4. This suggests targeting the YTHDF2-ACE/BMP4 pathway could treat microvascular diseases.

Area of Science:

  • Molecular Biology
  • Immunology
  • Ophthalmology

Background:

  • Microvascular dysfunction underlies severe diseases, with retinal microvascular issues causing blindness.
  • Aberrant microglia activation is implicated in microvasculopathies, but molecular drivers are unknown.
  • The role of N6-methyladenosine (m6A) modification in retinal vasculopathy remains unexplored.

Purpose of the Study:

  • Investigate the function of the m6A reader YTHDF2 in microglia.
  • Determine YTHDF2's role in retinal vasculopathy and its regulatory mechanisms.

Main Methods:

  • Assessed microglial YTHDF2 expression in oxygen-induced retinopathy (OIR) mice using single-cell RNA sequencing.
  • Generated microglia-specific Ythdf2 knockout mice to analyze retinal phenotypes.
  • Utilized RNA-seq and inhibitors to explore signaling pathways.

Main Results:

  • YTHDF2 was downregulated in microglia from diseased retinas.
  • Microglial Ythdf2 knockout impaired physiological angiogenesis and exacerbated pathological angiogenesis in OIR.
  • YTHDF2 directly controlled Ace and Bmp4 mRNA stability; Ace inhibition or Bmp4 antagonism ameliorated retinopathy.

Conclusions:

  • Loss of YTHDF2 in microglia promotes activation and microvascular anomalies via Ace and Bmp4.
  • This highlights the YTHDF2-Ace/Bmp4 network's importance in microvascular development and disease.
  • Targeting this network offers potential therapeutic strategies for microvascular diseases.
Keywords:
MicrogliaMicrovascular dysfunctionN(6)-methyladenosine (m(6)A) modificationYthdf2

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