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Decreasing mitochondrial fission ameliorates HIF-1α-dependent pathological retinal angiogenesis.

Shu-Qi Huang1, Kai-Xiang Cao1, Cai-Ling Wang1

  • 1School of Basic Medical Sciences; The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Guangzhou Medical University, Guangzhou, 511436, China.

Acta Pharmacologica Sinica
|April 2, 2024
PubMed
Summary

Targeting mitochondrial fission, driven by dynamin-related protein 1 (DRP1), can inhibit pathological angiogenesis in eye diseases. This approach reduces reactive oxygen species (ROS) production and shows promise for treating proliferative retinopathies.

Keywords:
Dynamin-related protein 1Mdivi-1ROS.glycolysismitochondrial fissionpathological angiogenesis

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Area of Science:

  • Cell Biology
  • Ophthalmology
  • Biochemistry

Background:

  • Angiogenesis is crucial in pathological processes like retinopathy of prematurity, a cause of blindness.
  • Endothelial mitochondria regulate angiogenesis via reactive oxygen species (ROS) and calcium signaling.
  • Mitochondrial dynamics, including fusion and fission, are key to these processes.

Purpose of the Study:

  • To investigate the role of mitochondrial dynamics in pathological retinal angiogenesis.
  • To explore the therapeutic potential of targeting mitochondrial fission in proliferative retinopathies.

Main Methods:

  • Used human umbilical vein endothelial cells (HUVECs) treated with vascular endothelial growth factor (VEGF).
  • Investigated the role of dynamin-related protein 1 (DRP1) and its inhibitor Mdivi-1.
  • Utilized an oxygen-induced retinopathy (OIR) mouse model.

Main Results:

  • VEGF induced mitochondrial fission in HUVECs via DRP1 phosphorylation.
  • DRP1 inhibition blocked VEGF-induced HUVEC migration, proliferation, and tube formation.
  • VEGF increased ROS production, essential for HIF-1α-dependent glycolysis and angiogenesis; inhibiting fission reduced ROS.
  • Active DRP1 was found in retinal neovascular tufts in OIR mice.
  • Mdivi-1 treatment significantly reduced pathological angiogenesis in the OIR model.

Conclusions:

  • Mitochondrial fission, regulated by DRP1, is a key driver of pathological angiogenesis.
  • Inhibiting mitochondrial fission reduces ROS production and alleviates neovascularization.
  • Targeting mitochondrial fission presents a potential therapeutic strategy for proliferative retinopathies and other angiogenesis-dependent diseases.