Long-chain acyl-CoA synthetase in fatty acid metabolism involved in liver and other diseases:An update

Long-chain acyl-Co A synthetase(ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form a...

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Published inWorld journal of gastroenterology : WJG Vol. 21; no. 12; pp. 3492 - 3498
Main Author Yan, Sheng
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Inc 28.03.2015
Subjects
acid;Prolife
acyl-Co
Animals
Apoptosis
Cell Proliferation
Coenzyme A Ligases - metabolism
Fatty Acids - metabolism
Humans
Isoenzymes
Liver - enzymology
Liver - pathology
Liver - physiopathology
Liver Diseases - enzymology
Liver Diseases - pathology
Liver Diseases - physiopathology
Long-chain
Metabolic Diseases - enzymology
Nervous System Diseases - enzymology
Review
Signal Transduction
synthetase;Fatty
Liver diseases
Pathways
Fatty acid
Metabolic diseases
Proliferation
Long-chain acyl-CoA synthetase
Apoptosis
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Summary:Long-chain acyl-Co A synthetase(ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form acyl-Co As, which are lipid metabolic intermediates and involved in fatty acid metabolism, membrane modifications and various physiological processes. Gain- or lossof-function studies have shown that the expression of individual ACSL isoforms can alter the distribution and amount of intracellular fatty acids. Changes in the types and amounts of fatty acids, in turn, can alter the expression of intracellular ACSLs. ACSL family members affect not only the proliferation of normal cells, but the proliferation of malignant tumor cells. They also regulate cell apoptosis through different signaling pathways and molecular mechanisms. ACSL members have individual functions in fatty acid metabolism in different types of cells depending on substrate preferences, subcellular location and tissue specificity, thus contributing to liver diseases and metabolic diseases, such as fatty liver disease, obesity, atherosclerosis and diabetes. They are also linked to neurological disorders and other diseases. However, the mechanisms are unclear. This review addresses new findings in the classification and properties of ACSLs and the fatty acid metabolismassociated effects of ACSLs in diseases.
Bibliography:Long-chain acyl-Co A synthetase;Fatty acid;Prolife
Long-chain acyl-Co A synthetase(ACSL) family members include five different ACSL isoforms, each encoded by a separate gene and have multiple spliced variants. ACSLs on endoplasmic reticulum and mitochondrial outer membrance catalyze fatty acids with chain lengths from 12 to 20 carbon atoms to form acyl-Co As, which are lipid metabolic intermediates and involved in fatty acid metabolism, membrane modifications and various physiological processes. Gain- or lossof-function studies have shown that the expression of individual ACSL isoforms can alter the distribution and amount of intracellular fatty acids. Changes in the types and amounts of fatty acids, in turn, can alter the expression of intracellular ACSLs. ACSL family members affect not only the proliferation of normal cells, but the proliferation of malignant tumor cells. They also regulate cell apoptosis through different signaling pathways and molecular mechanisms. ACSL members have individual functions in fatty acid metabolism in different types of cells depending on substrate preferences, subcellular location and tissue specificity, thus contributing to liver diseases and metabolic diseases, such as fatty liver disease, obesity, atherosclerosis and diabetes. They are also linked to neurological disorders and other diseases. However, the mechanisms are unclear. This review addresses new findings in the classification and properties of ACSLs and the fatty acid metabolismassociated effects of ACSLs in diseases.
Sheng Yan;Xue-Feng Yang;Hao-Lei Liu;Nian Fu;Yan Ouyang;Kai Qing;Department of Gastroenterology, Affiliated Nanhua Hospital of University of South China;Department of Nephrology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine;Department of Hematology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine
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Author contributions: Yang XF designed the paper; Yan S performed research of literature data and wrote the paper; Liu HL wrote the paper; Fu N performed research of literature data and revised the paper; Ouyang Y and Qing K revised the paper.
Correspondence to: Xue-Feng Yang, Professor, Department of Gastroenterology, Affiliated Nanhua Hospital of University of South China, No. 336, South Dongfeng Road, Hengyang 421001, Hunan Province, China. yxf9988@126.com
Telephone: +86-734-8358399 Fax: +86-734-8358399
ISSN:1007-9327
2219-2840
2219-2840
DOI:10.3748/wjg.v21.i12.3492