期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 93, 期 -, 页码 312-321出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2021.01.003
关键词
ACSL4; Ischemic stroke; Ferroptosis; Neuroinflammation
资金
- National Natural Science Foundation of China [31900634]
- Clinical Medicine + X Scientific Research Project of the Affiliated Hospital of Qingdao University
ACSL4 is an important regulator of neuronal death and neuroinflammation in ischemic stroke, with its suppression protecting mice against brain ischemia and promoting neuronal death via enhancing lipid peroxidation. Additionally, knockdown of ACSL4 can inhibit proinflammatory cytokine production in microglia.
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-1?. 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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