Regulation and role of Acyl-CoA synthetase 4 in glial cells

Dattilo, Melina Andrea; Benzo, Yanina; Herrera, Lucía Manuela; Prada, Jesica Giselle; Lopez, Paula; Caruso, Carla Mariana; Lasaga, Mercedes; Paz, Cristina; Maloberti, Paula

doi:10.1016/j.jsbmb.2020.105792

Cited by 3 publications

(5 citation statements)

References 60 publications

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“…Finally, AA-CoA is converted back into free AA and CoA by mitochondrial acyl-CoA thioesterase [104–106] . Under c-AMP stimulation, ACSL4 inhibition could reduce both the mRNA and protein levels of StAR, leading to disturbed steroid biosynthesis [104,107,108] . A possible explanation is that ACSL4 depletion could attenuate the promoting effect of AA and its metabolites on StAR expression by blocking the translocation of AA from the cytoplasm to mitochondria [104] .…”

Section: Biological Function Of Acsl4mentioning

confidence: 99%

“…[104][105][106] Under c-AMP stimulation, ACSL4 inhibition could reduce both the mRNA and protein levels of StAR, leading to disturbed steroid biosynthesis. [104,107,108] A possible explanation is that ACSL4 depletion could attenuate the promoting effect of AA and its metabolites on StAR expression by blocking the translocation of AA from the cytoplasm to mitochondria. [104] In addition, ACSL4 deficiency could reduce intracellular cholesteryl ester storage and, thus, decrease steroidogenesis.…”

Section: Remodeling the Pl Compositionmentioning

confidence: 99%

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

Ding

Liu

et al. 2023

Chinese Medical Journal

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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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Section: Biological Function Of Acsl4mentioning

confidence: 99%

Section: Remodeling the Pl Compositionmentioning

confidence: 99%

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

Ding

Liu

et al. 2023

Chinese Medical Journal

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“…In the present study, researchers found that ACSL4 promoted ferroptosis in glioma cells and functioned with anti-proliferative effects [ 55 ]. The depletion of ACSL4 reportedly reduces tumor necrosis, proliferation, migration, and cell self-renewal ability [ 56 , 57 ]. In a study that used erastin treatment to increase ACSL4 levels, heat shock protein 90 (Hsp90)–dynamin-related protein 1 (Drp1)–Acsl4 upregulation actively regulates ferroptosis by generating lipid ROS and altering mitochondrial morphology [ 58 ].…”

Section: Acsl3 and Acsl4 In Cancersmentioning

confidence: 99%

ACSL3 and ACSL4, Distinct Roles in Ferroptosis and Cancers

Yang

Zhu

Wang

et al. 2022

Cancers

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The long-chain fatty acyl CoA synthetase (ACSLs) family of enzymes contributes significantly to lipid metabolism and produces acyl-coenzyme A by catalyzing fatty acid oxidation. The dysregulation of ACSL3 and ACSL4, which belong to the five isoforms of ACSLs, plays a key role in cancer initiation, development, metastasis, and tumor immunity and may provide several possible therapeutic strategies. Moreover, ACSL3 and ACSL4 are crucial for ferroptosis, a non-apoptotic cell death triggered by the accumulation of membrane lipid peroxides due to iron overload. Here, we present a summary of the current knowledge on ACSL3 and ACSL4 and their functions in various cancers. Research on the molecular mechanisms involved in the regulation of ferroptosis is critical to developing targeted therapies for cancer.

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“…Modulates prostaglandin E2 secretion. Preferred substrates: arachidonate (Klett et al, 2017) Central nervous system Glioma (Zhou et al, 2019;Cheng et al, 2020;Tan et al, 2020;Yee et al, 2020;Yi et al, 2020;Dattilo et al, 2021;Hacioglu and Kar, 2022;Kram et al, 2022;Miao et al, 2022) Cerebrovascular diseases: ischemic stroke (Gubern et al, 2013;Li et al, 2019;Chen J. et al, 2021;Cui et al, 2021;Guo H. et al, 2021;Li C. et al, 2021;Liao et al, 2021;Tuo et al, 2022), hemorrhage (Chen B. et al, 2021;Jin et al, 2021), subarachnoid hemorrhage (Qu et al, 2021;Huang et al, 2022;Yuan et al, 2022) Injury: traumatic brain injury (Kenny et al, 2019;Xiao et al, 2019;Bao Z. et al, 2021), spinal cord injury (Zhou et al, 2020;Pang et al, 2022) Intellectual disability: non-syndromic X-Linked intellectual developmental disorder (Meloni et al, 2009;Zhang et al, 2009;Liu et al, 2011Liu et al, , 2014Huang et al, 2016;Chang et al, 2019;Jia et al, 2019), Alport syndrome with intellectual disability (Rodriguez et al, 2010;Smetana et al, 2021) Neurodegenerative diseases: Alzheimer's disease (AD) (Rapoport, 2008;…”

Section: Gliomamentioning

confidence: 99%

“…Numerous glioma-associated studies have focused on the determination of ferroptosis-related protein expression, such as ACSL4, glutathione peroxidase (GPX4), system Xc – , and ferroptosis suppressor protein 1/AIFM2 (FSP1), etc. Mechanistically, ACSL4 is required for ferroptosis in glioma via the regulation of proliferation, migration of glioblastoma, and self-renewal of glia cells ( Cheng et al, 2020 ; Bao C. et al, 2021 ; Dattilo et al, 2021 ). The decrease in the expression level of ACSL4 has been observed in isocitrate dehydrogenase (IDH) 1 wild-type and mutant gliomas ( Zhou et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

An update on the therapeutic implications of long-chain acyl-coenzyme A synthetases in nervous system diseases

Sun

et al. 2022

Front. Neurosci.

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Long-chain acyl-coenzyme A synthetases (ACSLs) are a family of CoA synthetases that activate fatty acid (FA) with chain lengths of 12–20 carbon atoms by forming the acyl-AMP derivative in an isozyme-specific manner. This family mainly includes five members (ACSL1, ACSL3, ACSL4, ACSL5, and ACSL6), which are thought to have specific and different functions in FA metabolism and oxidative stress of mammals. Accumulating evidence shows that the dysfunction of ACSLs is likely to affect cell proliferation and lead to metabolic diseases in multiple organs and systems through different signaling pathways and molecular mechanisms. Hence, a central theme of this review is to emphasize the therapeutic implications of ACSLs in nervous system disorders.

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Regulation and role of Acyl-CoA synthetase 4 in glial cells

Cited by 3 publications

References 60 publications

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

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

ACSL3 and ACSL4, Distinct Roles in Ferroptosis and Cancers

An update on the therapeutic implications of long-chain acyl-coenzyme A synthetases in nervous system diseases

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