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Updated: Feb 8, 2026

Induction of Retinal Ischemia-Reperfusion Injury in a Mouse Eye Model
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ACSL4 Inhibition by AS-252424 Protects Visual Function by Suppressing RGC Ferroptosis After Retinal Ischemia

Keyu Liu1, Zihao Lin2, Wu Xiang2

  • 1Department of Ophthalmology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, #107 Wenhuaxi Road, Jinan, 250014, China.

Molecular Neurobiology
|February 6, 2026
PubMed
Summary
This summary is machine-generated.

AS-252424, an acyl-CoA synthetase long-chain family member 4 (ACSL4) inhibitor, protects retinal ganglion cells from ischemia-reperfusion injury by reducing ferroptosis. This neuroprotective strategy preserves retinal structure and visual function.

Keywords:
ACSL4AS-252424NeuroprotectionRetinal ischemia–reperfusion

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Area of Science:

  • Ophthalmology
  • Neuroscience
  • Molecular Biology

Background:

  • Retinal ischemia-reperfusion (IR) injury causes significant vision loss.
  • Acyl-CoA synthetase long-chain family member 4 (ACSL4) plays a role in ferroptosis, a form of regulated cell death.
  • Targeting ACSL4 may offer a novel therapeutic approach for retinal injury.

Purpose of the Study:

  • To investigate the neuroprotective effects of AS-252424, a selective ACSL4 inhibitor, against retinal IR injury.
  • To elucidate the underlying mechanisms of AS-252424's action, focusing on ferroptosis.
  • To assess the impact of AS-252424 on retinal structure, function, and cell survival.

Main Methods:

  • Establishment of a mouse model of retinal IR.
  • Intravitreal administration of AS-252424 to assess neuroprotection.
  • Evaluation of retinal ganglion cell (RGC) survival, retinal morphology, and function (electroretinography).
  • Measurement of ACSL4 expression, localization, enzymatic activity, and ferroptotic markers.

Main Results:

  • AS-252424 significantly reduced RGC loss and preserved inner retinal integrity after IR.
  • AS-252424 treatment restored retinal function, including a-wave, b-wave, and oscillatory potentials.
  • The drug inhibited ACSL4-mediated lipid peroxidation and ferroptosis by lowering arachidonic acid-CoA levels.
  • AS-252424 demonstrated comparable RGC protection to Fer-1 at a lower concentration.

Conclusions:

  • AS-252424 provides significant neuroprotection against retinal IR injury.
  • The mechanism involves the inhibition of ACSL4-mediated ferroptosis.
  • Targeting ACSL4 is a promising strategy for preserving visual function in ischemic retinopathy.