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ACSL4 exacerbates ischemic stroke by promoting ferroptosis-induced brain injury and neuroinflammation.

Author information

Affiliations

  • 1. Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, Ningxia Road 308, Qingdao 266071, Shandong, China.
      Authors
    • Cui Y 1
    (1 author)
  • 2. Department of Interventional Radiology, The Affiliated Hospital of Qingdao University, Jiangsu Road 16, Qingdao 266000, Shandong, China.
      Authors
    • Zhang Y 2
    • Zhao X 2
    • Shao L 2
    • Liu G 2
    • Sun C 2
    • Xu R 2
    • Zhang Z 2
    (7 authors)

ORCIDs linked to this article

Brain, Behavior, and Immunity, 11 Jan 2021, 93:312-321
https://doi.org/10.1016/j.bbi.2021.01.003 PMID: 33444733 

Abstract 

Acyl-CoA synthetase long-chain family member 4 (ACSL4) is an important isozyme for polyunsaturated fatty acids (PUFAs) metabolism that dictates ferroptosis sensitivity. The role of ACSL4 in the progression of ischemic stroke is unclear. Here, we found that ACSL4 expression was suppressed in the early phase of ischemic stroke and this suppression was induced by HIF-1α. Knockdown of ACSL4 protected mice against brain ischemia, whereas, forced overexpression of ACSL4 exacerbated ischemic brain injury. ACSL4 promoted neuronal death via enhancing lipid peroxidation, a marker of ferroptosis. Moreover, knockdown of ACSL4 inhibited proinflammatory cytokine production in microglia. These data identify ACSL4 as a novel regulator of neuronal death and neuroinflammation, and interventions of ACSL4 expression may provide a potential therapeutic target in ischemic stroke.

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Read article at publisher's site: https://doi.org/10.1016/j.bbi.2021.01.003

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Funding 

Funders who supported this work.

National Natural Science Foundation of China (1)

Qingdao University