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FUNDC1 Induces Apoptosis and Autophagy Under Oxidative Stress via PI3K/Akt/mTOR Pathway in Cataract Lens Cells

Duo Dong1, Jing Wu1, Lijie Sheng1

  • 1Department of Ophthalmology, The Second Affiliated Hospital of Qiqihar Medical College, Qiqihar, China.

Current Eye Research
|February 18, 2022
PubMed
Abstract

Insights

FUNDC1 deficiency restrains cataract cell apoptosis and autophagy by inhibiting the PI3K/Akt/mTOR pathway. This finding offers new insights into cataract mechanisms and potential therapeutic targets.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • Cataracts are a leading cause of blindness, often associated with oxidative stress in lens cells.
  • Understanding the molecular mechanisms underlying cataract formation is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the expression of FUNDC1 in cataract cells and tissues.
  • To elucidate the role and mechanism of FUNDC1 in cataract development under oxidative stress.

Main Methods:

  • Bioinformatic analysis of gene expression data (GSE153933).
  • Quantitative PCR and Western blotting to measure FUNDC1 expression.
  • Methylation-specific PCR to assess promoter methylation.
  • Flow cytometry for apoptosis assays.
  • Immunofluorescence and Western blotting for autophagy and signaling pathway analysis.

Main Results:

  • FUNDC1 was upregulated in cataract cells and tissues.
  • FUNDC1 expression increased under oxidative stress (H2O2), with hypomethylation of its promoter.
  • FUNDC1 knockdown reduced apoptosis and autophagy; overexpression increased them.
  • FUNDC1 inhibited the PI3K/Akt/mTOR pathway phosphorylation.

Conclusions:

  • FUNDC1 plays a significant role in regulating apoptosis and autophagy in cataract cells.
  • FUNDC1 deficiency restrains cell apoptosis and autophagy by inhibiting the PI3K/Akt/mTOR signaling pathway.
  • FUNDC1 represents a potential therapeutic target for cataract treatment.
Keywords:
FUNDC1PI3K/Akt/mTORautophagycell apoptosisoxidative stress

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