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Cited by 396Ferroptosis and cancer prognosisCancer, Lipids, and MetabolismLipid metabolism and biosynthesis

Acyl-CoA synthase ACSL4: an essential target in ferroptosis and fatty acid metabolism

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Ding, Kaiyue, Liu, Chongbin, Li, Li, Yang, Ming, Jiang, Na, Luo, Shilu, Sun, Lin·2023·Chinese Medical Journal
DOI 10.1097/cm9.0000000000002533PMC PMC10617883
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Abstract

Long-chain acyl-coenzyme A (CoA) synthase 4 (ACSL4) is an enzyme that esterifies CoA into specific polyunsaturated fatty acids, such as arachidonic acid and adrenic acid. Based on accumulated evidence, the ACSL4-catalyzed biosynthesis of arachidonoyl-CoA contributes to the execution of ferroptosis by triggering phospholipid peroxidation. Ferroptosis is a type of programmed cell death caused by iron-dependent peroxidation of lipids; ACSL4 and glutathione peroxidase 4 positively and negatively regulate ferroptosis, respectively. In addition, ACSL4 is an essential regulator of fatty acid (FA) metabolism. ACSL4 remodels the phospholipid composition of cell membranes, regulates steroidogenesis, and balances eicosanoid biosynthesis. In addition, ACSL4-mediated metabolic reprogramming and antitumor immunity have attracted much attention in cancer biology. Because it facilitates the cross-talk between ferroptosis and FA metabolism, ACSL4 is also a research hotspot in metabolic diseases and ischemia/reperfusion injuries. In this review, we focus on the structure, biological function, and unique role of ASCL4 in various human diseases. Finally, we propose that ACSL4 might be a potential therapeutic target.

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  • Rosiglitazone is an inhibitor of acyl-CoA synthetase long-chain family member 4 (ACSL4), an enzyme that catalyzes the esterification of arachidonic and adrenic acids preparing them for synthesis of phospholipids, enriching membranes with oxidizable polyunsaturated fatty acids and thereby promoting the LPO that drives ferroptosis.

    “In addition, we tested rosiglitazone, an inhibitor of acyl-CoA synthetase long-chain family member 4 (ACSL4), an enzyme that catalyzes the esterification of arachidonic and adrenic acids preparing them for synthesis of phospholipids, enriching membranes with oxidizable polyunsaturated fatty acids and thereby promoting the LPO that drives ferroptosis (Ding et al., 2023).”

    From Toxic Concentrations of Glutamate Induce Ferroptosis without Affecting Mitochondrial Respiration in Rodent Brain Slice Cultures (2026) · cites this paper as Ding et al., 2023

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Cited by

Sorted by citations

Authors
Ding, K., Liu, C., Li, L., Yang, M., Jiang, N., Luo, S., & Sun, L.
Affiliations
Central South University (CN)
Corresponding author
  • Li, Li
  • Sun, Lin
ORCID
Venue
Chinese Medical Journal
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2023-07-05
Volume
136
Issue
21
Pages
2521-2537
ISSN
  • 0366-6999 (ISSN-L)
  • 2542-5641
DOI
10.1097/cm9.0000000000002533
PMC
PMC10617883
OpenAlex
W4384155944
Cited by
396
References
9
Citations by year
2026: 181 · 2025: 168 · 2024: 45 · 2023: 2
FWCI
17.58
Type
journal article
Language
en
Open access
Licence
Locations
  • Chinese Medical Journal (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Natural Science Foundation of China (81730018)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
ACSL4, ferroptosis, fatty acid metabolism, arachidonoyl-CoA, phospholipid peroxidation, GPX4, eicosanoid biosynthesis, steroidogenesis, membrane lipid remodeling, metabolic reprogramming, antitumor immunity, ischemia-reperfusion injury, therapeutic target
MeSH terms
Ferroptosis, Humans, Phospholipids, Apoptosis, Nitric Oxide Synthase

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