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FUNDC1 deficiency aggravates endothelial senescence and retinal dysfunction.

Jingxin Ning1, Ze Li2, Yuxue Mu3

  • 1College of Life Sciences, Northwest University, Xi'an, 710069, China; National Demonstration Center for Experimental Basic Medical Science Education, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|October 24, 2025
PubMed
Summary

Reduced FUNDC1 expression in retinal endothelial cells impairs mitophagy and worsens age-related vision decline. Restoring FUNDC1 may prevent or treat retinal degeneration.

Keywords:
Endothelial senescenceFUNDC1MitophagyROSRetinal vessels

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Area of Science:

  • Ophthalmology
  • Gerontology
  • Cell Biology

Background:

  • Aging impairs visual function and causes ocular diseases, with endothelial cell aging contributing to retinal degeneration.
  • Mitochondrial homeostasis is crucial for endothelial cell function, and mitophagy removes damaged mitochondria. FUNDC1 is a key mitophagy receptor.
  • Mechanisms linking endothelial cell aging to retinopathy, particularly involving mitochondrial imbalance and FUNDC1, are not fully understood.

Purpose of the Study:

  • To investigate the role of FUNDC1-mediated mitophagy in age-related decline of retinal vascular and overall function.
  • To determine if reduced FUNDC1 expression in retinal endothelial cells contributes to mitochondrial dysfunction and vascular aging.
  • To explore FUNDC1 as a potential therapeutic target for age-related retinal degeneration.

Main Methods:

  • Examined FUNDC1 expression, mitophagy levels, and retinal vascular function in aged mice.
  • Utilized fluorescein fundus angiography and electron microscopy to assess vascular permeability and mitochondrial morphology.
  • Investigated the effects of endothelial-specific FUNDC1 knockout and D-galactose-induced senescence in cell models.

Main Results:

  • Aged mice showed decreased FUNDC1 expression and mitophagy in retinal blood vessels, alongside increased vascular permeability and mitochondrial swelling.
  • Endothelial FUNDC1 knockout exacerbated age-related retinal dysfunction; D-galactose-induced senescence impaired mitophagy and increased endothelial permeability.
  • FUNDC1 overexpression reversed age-related mitochondrial dysfunction, junctional protein loss, and endothelial hyperpermeability.

Conclusions:

  • FUNDC1 deficiency exacerbates age-related retinal vascular dysfunction and functional decline by impairing mitophagy and mitochondrial homeostasis.
  • FUNDC1 plays a critical role in maintaining retinal endothelial cell function during aging.
  • FUNDC1 represents a promising therapeutic target for preventing and treating age-related retinal degeneration.