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

被引：115
作者：
Ding, Kaiyue [1 ,2 ]
Liu, Chongbin [1 ,2 ]
Li, Li [1 ,2 ]
Yang, Ming [1 ,2 ]
Jiang, Na [1 ,2 ]
Luo, Shilu [1 ,2 ]
Sun, Lin [1 ,2 ]
机构：
[1] Cent South Univ, Xiangya Hosp 2, Dept Nephrol, Changsha 410000, Hunan, Peoples R China
[2] Hunan Key Lab Kidney Dis & Blood Purificat, Changsha 410000, Hunan, Peoples R China
来源：
CHINESE MEDICAL JOURNAL | 2023年 / 136卷 / 21期
基金：
中国国家自然科学基金;
关键词：
Long-chain acyl-coenzyme A (CoA) synthase 4 (ACSL4); Ferroptosis; Fatty acid metabolism; Cancer; Ischemia/reperfusion; Metabolic diseases; SYNTHETASE; 4; EXPRESSION; ARACHIDONIC-ACID; COLORECTAL-CANCER; STIMULATED STEROIDOGENESIS; HEPATOCELLULAR-CARCINOMA; PROTEIN EXPRESSION; PANCREATIC-CANCER; LIPID-METABOLISM; BREAST-CANCER; IRON UPTAKE;
D O I：
10.1097/CM9.0000000000002533
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
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.
引用
收藏
页码：2521 / 2537
页数：17
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