Biochimica et biophysica acta. Molecular and cell biology of lipids最新文献_第3页

Different effects of Lorenzo's oil components against very long-chain fatty acid-induced endoplasmic reticulum stress in peroxisome-deficient CHO cells 在过氧化物酶体缺乏的CHO细胞中，洛伦佐油成分对长链脂肪酸诱导的内质网应激的不同影响。

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-27 DOI: 10.1016/j.bbalip.2025.159670

Hanif Ali , Mone Yamanishi , Rumana Yesmin Hasi , Majidul Islam , Yoshimasa Hamada , Masato Miyake , Seiichi Oyadomari , Emi Kiyokage , Kazunori Toida , Ryushi Kawakami , Mutsumi Aihara , Tamotsu Tanaka

{"title":"Different effects of Lorenzo's oil components against very long-chain fatty acid-induced endoplasmic reticulum stress in peroxisome-deficient CHO cells","authors":"Hanif Ali , Mone Yamanishi , Rumana Yesmin Hasi , Majidul Islam , Yoshimasa Hamada , Masato Miyake , Seiichi Oyadomari , Emi Kiyokage , Kazunori Toida , Ryushi Kawakami , Mutsumi Aihara , Tamotsu Tanaka","doi":"10.1016/j.bbalip.2025.159670","DOIUrl":"10.1016/j.bbalip.2025.159670","url":null,"abstract":"<div><div>Adrenoleukodystrophy (ALD) is an X-linked peroxisomal disorder caused by mutations in the <em>ABCD1</em> gene, leading to the accumulation of very long-chain fatty acids (VLCFAs). The accumulation of saturated VLCFAs, such as C24:0 and C26:0, is believed to impair myelination. A mixture of C18:1 (oleic acid) and C22:1 (erucic acid), known as Lorenzo's oil, has been used to reduce these saturated VLCFAs. However, despite lowering saturated VLCFA levels, Lorenzo's oil proved ineffective in preventing neurological symptoms. Previously, we found that VLCFA-induced apoptosis is prevented by C18:1 supplementation in peroxisome-deficient Chinese Hamster Overy (CHO) cells. In this study, we investigated the mechanism underlying the rescue effect of C18:1 and examined the effect of C22:1, another component of Lorenzo's oil. Supplementation with C18:1 completely rescued the cells from VLCFA-induced apoptosis. In contrast, C22:1 enhanced VLCFA cytotoxicity and diminished the protective effect of C18:1. We found that VLCFA-induced apoptosis is mediated via the endoplasmic reticulum (ER) stress response possibly by disruption of ER structure, whereas C18:1 attenuated this ER stress. Quantitative lipidomics revealed that VLCFAs were predominantly incorporated into phosphatidylcholine (PC), accompanied by a significant reduction in PC species containing C18:1. Among these, PC 36:2 (18:1/18:1) showed a pattern of change that correlated with cellular viability. These results indicate that C18:1, but not C22:1, protects peroxisome-deficient CHO cells by ameliorating the ER stress response, likely through improving ER structure distorted by VLCFA accumulation.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159670"},"PeriodicalIF":3.3,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144741062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phosphoinositides as regulators of membrane contact sites 磷酸肌苷作为膜接触位点的调节剂。

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-26 DOI: 10.1016/j.bbalip.2025.159673

Håvard S. Haukaas , Harald Stenmark

引用次数: 0

ABCA1 modifies plasma membrane organization of living cells ABCA1修饰活细胞的质膜组织

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-26 DOI: 10.1016/j.bbalip.2025.159667

Mateusz Kondratowicz , Ambroise Wu , Ewa Grela , Olga Raducka-Jaszul , Rafał Luchowski , Ewa Błaszczak , Karolina Wójtowicz , Yannick Hamon , Wiesław I. Gruszecki , Katarzyna Cieślik-Boczula , Tomasz Trombik

{"title":"ABCA1 modifies plasma membrane organization of living cells","authors":"Mateusz Kondratowicz , Ambroise Wu , Ewa Grela , Olga Raducka-Jaszul , Rafał Luchowski , Ewa Błaszczak , Karolina Wójtowicz , Yannick Hamon , Wiesław I. Gruszecki , Katarzyna Cieślik-Boczula , Tomasz Trombik","doi":"10.1016/j.bbalip.2025.159667","DOIUrl":"10.1016/j.bbalip.2025.159667","url":null,"abstract":"<div><div>The plasma membrane, composed mostly of lipids and proteins, is a dynamic structure essential for maintaining cellular homeostasis and signaling. Its composition, organization and molecular dynamics have important functional consequences for the cell, while aberrations of its integrity are associated with various human pathologies, including cancers, inflammatory and neurodegenerative diseases. ATP-binding cassette transporter A1 (ABCA1) plays a key role in cellular lipid and cholesterol metabolism, yet its impact on plasma membrane organization and dynamics remains incompletely understood. Using multidisciplinary approaches, we investigated how ABCA1 activity alters plasma membrane dynamics and nanodomain organization in living cells. Fluorescence lifetime imaging microscopy (FLIM) and fluorescence anisotropy showed that active ABCA1 increases membrane homogeneity. Proton nuclear magnetic resonance (<sup>1</sup>H NMR) spectroscopy of living cells demonstrated that ABCA1 activity alters membrane fluidity and induces its distinct chemical composition changes. Furthermore, spot variation fluorescence correlation spectroscopy (svFCS) revealed that ABCA1 modulates lipid and protein diffusion dynamics. Our findings confirm and extend previous studies by demonstrating that ABCA1 is one of the key regulators of plasma membrane lipid distribution, influencing its structural and functional organization. By modulating lipid-raft nanodomains, ABCA1 activity may have broader implications for membrane-dependent cellular processes.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159667"},"PeriodicalIF":3.3,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144724859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Control of ALOX5 expression in monocytic cells using a synthetic riboswitch 利用合成核糖开关控制ALOX5在单核细胞中的表达

IF 3.9 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-25 DOI: 10.1016/j.bbalip.2025.159671

Robin W. Bruckhoff , Julia H. Oberlis , Dieter Steinhilber , Beatrix Suess

{"title":"Control of ALOX5 expression in monocytic cells using a synthetic riboswitch","authors":"Robin W. Bruckhoff , Julia H. Oberlis , Dieter Steinhilber , Beatrix Suess","doi":"10.1016/j.bbalip.2025.159671","DOIUrl":"10.1016/j.bbalip.2025.159671","url":null,"abstract":"<div><div>The human 5-lipoxygenase (5-LOX), which is encoded by the arachidonate 5-lipoxygenase (<em>ALOX5</em>) gene, has its canonical function in leukotriene (LT) biosynthesis, which controls inflammatory and allergic responses. Besides oxylipin formation from polyunsaturated fatty acids, 5-LOX has several noncanonical functions. It acts as transcriptional regulator in the nucleus but also interacts with Dicer and modulates microRNA expression and processing.</div><div>In this study, we employed a tetracycline riboswitch-controlled cassette-exon system to conditionally control <em>ALOX5</em> expression in the monocytic leukemic cell line MonoMac6. Synthetic riboswitches are gaining increasing interest as a means of controlling transgene expression, with applications in functional genomics and potential therapeutic strategies. We designed an artificial <em>ALOX5</em> gene that contains two cassette exons with premature termination codons (PTCs), thus only being expressed when both synthetic exons are skipped. The switchable <em>ALOX5</em> gene was transduced into MonoMac6 5-LOX knock-out (KO) cells, thereby enabling the tetracycline-dependent re-expression of 5-LOX proteins. The newly established cell line was characterized in terms of tetracycline dose dependency and switching kinetics. Induction of <em>ALOX5</em> exerted the non-canonical 5-LOX effects on prostaglandin-endoperoxide synthase 2 (<em>PTGS2</em>) and L-kynureninase (<em>KYNU</em>) gene expression. This allowed us to demonstrate the outstanding advantages of a riboswitch-controlled system in terms of time dependency and gene function. The novel MonoMac6 cell line now provides a perfect tool for further research into the non-canonical functions of 5-LOX.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159671"},"PeriodicalIF":3.9,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144714089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polyunsaturated fatty acids in kidney diseases: Navigating the fine line between healing and damage 多不饱和脂肪酸在肾脏疾病中：在愈合和损害之间的细线上导航。

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-23 DOI: 10.1016/j.bbalip.2025.159668

Mehrdad Aghasizadeh , Ahmad Reza Bahrami , Maryam M. Matin

{"title":"Polyunsaturated fatty acids in kidney diseases: Navigating the fine line between healing and damage","authors":"Mehrdad Aghasizadeh , Ahmad Reza Bahrami , Maryam M. Matin","doi":"10.1016/j.bbalip.2025.159668","DOIUrl":"10.1016/j.bbalip.2025.159668","url":null,"abstract":"<div><div>Polyunsaturated fatty acids (PUFAs) regulate renal inflammation through metabolites generated by COX, LOX, and CYP pathways. While prostaglandins, leukotrienes, and 20-hydroxyeicosatetraenoic acid (20-HETE) exacerbate kidney injury, epoxyeicosatrienoic acids (EETs), lipoxins, and other specialized pro-resolving mediators (SPMs) counteract inflammation and promote tissue repair. These lipid mediators also modulate nuclear receptors such as peroxisome proliferator-activated receptors (PPARs) and fibrotic pathways like TGF-β signaling. Disease-specific imbalances in PUFA metabolism have been implicated in nephrotic syndrome, glomerulonephritis, kidney transplantation, and renal cancer. This review integrates mechanistic insights with experimental and clinical data, highlighting therapeutic strategies including dietary ω-3 PUFA supplementation, synthetic SPM analogs, selective enzyme inhibitors, and nanocarrier-based delivery systems. We also address limitations, such as short half-life, off-target effects, and immunoregulatory risks. Lipidomic profiling may aid in patient stratification and treatment personalization. Collectively, targeting PUFA-derived lipid mediators offers a promising adjunct to conventional therapies for inflammatory and immune-mediated kidney diseases.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159668"},"PeriodicalIF":3.3,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Linarin alleviates high-fat diet-induced NAFLD via modulating the PI3K/Akt/mTOR pathway, autophagy, and gut microbiota Linarin通过调节PI3K/Akt/mTOR通路、自噬和肠道微生物群来缓解高脂肪饮食诱导的NAFLD。

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-16 DOI: 10.1016/j.bbalip.2025.159666

Mengfan Lv , Yaxin Zhai , Hao Yu , Jiaqi Cheng , Yunfei Wei , Yibo Zhang , Yanmin Zhang , Haihua Feng

{"title":"Linarin alleviates high-fat diet-induced NAFLD via modulating the PI3K/Akt/mTOR pathway, autophagy, and gut microbiota","authors":"Mengfan Lv , Yaxin Zhai , Hao Yu , Jiaqi Cheng , Yunfei Wei , Yibo Zhang , Yanmin Zhang , Haihua Feng","doi":"10.1016/j.bbalip.2025.159666","DOIUrl":"10.1016/j.bbalip.2025.159666","url":null,"abstract":"<div><div>Linarin (Lin) is a flavonoid compound widely found in traditional herbal medicines and is recognized for its diverse biological properties, including anti-inflammatory, analgesic, antioxidant, hepatoprotective, and anti-apoptotic effects. Non-alcoholic fatty liver disease (NAFLD) is closely associated with autophagy and inflammation processes. However, the interaction between Lin and NAFLD remains underexplored. This study aimed to investigate the protective effects of Lin against NAFLD and its underlying pharmacological mechanisms. In vitro, we established a NAFLD model using AML12 cells stimulated with oleic acid (OA) and palmitic acid (PA). In vivo, we induced a chronic model in mice by feeding them a high-fat diet (HFD). Lipid metabolism markers, Oil Red O staining, and H&E staining were used to assess intracellular lipid accumulation. Inflammatory and autophagic markers were also measured. The 16S rRNA analysis was performed to evaluate the changes in the gut microbiota composition after Lin intervention in mice. Both in vitro and in vivo experiments demonstrated that Lin reduces lipid accumulation, which is mediated through the enhancement of autophagy and the inhibition of the release of inflammatory factors. 16S rRNA analysis revealed that Lin alleviates gut dysbiosis by reducing Firmicutes and Bacteroidetes phyla while increasing the abundance of Akkermansia and Bifidobacterium genera. Mechanistically, Lin activates autophagy via the PI3K/Akt/mTOR pathway, thereby alleviating lipid accumulation and inflammation. These findings suggest that Lin can mitigate NAFLD by inhibiting the activation of the PI3K/Akt/mTOR pathway, highlighting its potential as a promising therapeutic approach for NAFLD.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159666"},"PeriodicalIF":3.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of α-ketoglutarate on maternal lipid homeostasis and mitochondrial status perturbed by gestational arsenic exposure α-酮戊二酸对妊娠期砷暴露扰乱的母体脂质稳态和线粒体状态的影响

IF 3.9 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-16 DOI: 10.1016/j.bbalip.2025.159665

Tong Zhan , Shuang-Rui Bao , Ying Sun , Hong-Yan Wu , Wen-Kang Tao , Xin-Ru Liang , Zhi-Yan Wan , Qian Yang , Hua Wang , Yi-Chao Huang , Jian-Qing Wang , De-Xiang Xu , Cheng Zhang

{"title":"Effect of α-ketoglutarate on maternal lipid homeostasis and mitochondrial status perturbed by gestational arsenic exposure","authors":"Tong Zhan , Shuang-Rui Bao , Ying Sun , Hong-Yan Wu , Wen-Kang Tao , Xin-Ru Liang , Zhi-Yan Wan , Qian Yang , Hua Wang , Yi-Chao Huang , Jian-Qing Wang , De-Xiang Xu , Cheng Zhang","doi":"10.1016/j.bbalip.2025.159665","DOIUrl":"10.1016/j.bbalip.2025.159665","url":null,"abstract":"<div><div>Arsenic is a common environmental toxicant with known hepatotoxic effects, yet its impact on maternal lipid metabolism during pregnancy remains poorly understood. In this study, we established a pregnant mouse model to investigate the effects of gestational arsenic exposure and the potential protective role of α-ketoglutarate (α-KG), a key tricarboxylic acid (TCA) cycle intermediate. In the first experiment, arsenic exposure led to significant disruptions in maternal serum and hepatic lipid profiles. Mechanistically, arsenic reduced hepatic α-KG concentrations, impaired mitochondrial ultrastructure, altered mitochondria-related gene expression, induced oxidative stress, and decreased multiple TCA cycle intermediates, collectively indicating compromised mitochondrial function. In the second experiment, α-KG supplementation during gestation effectively restored hepatic α-KG levels and reversed arsenic-induced lipid metabolic imbalances. Moreover, α-KG preserved mitochondrial morphology, normalized the expression of mitochondrial genes, alleviated oxidative stress, and partially rescued the levels of disrupted TCA intermediates. These results suggest that arsenic disrupts maternal lipid homeostasis primarily through mitochondrial dysfunction and oxidative stress, and that α-KG supplementation can alleviate these disturbances by supporting mitochondrial function. Although the exact molecular mechanisms require further clarification, our findings highlight the potential therapeutic role of α-KG in maintaining maternal lipid metabolic health during arsenic exposure during pregnancy.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159665"},"PeriodicalIF":3.9,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144654420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metformin promotes lipid droplet-mitochondria coupling and improves insulin secretion in pancreatic β-cells exposed to lipotoxicity 二甲双胍促进脂滴-线粒体偶联并改善脂肪毒性胰腺β细胞的胰岛素分泌。

IF 3.9 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-12 DOI: 10.1016/j.bbalip.2025.159664

Aneta M. Dobosz , Ewelina Krogulec , Nataniel Stefanowski , Maria Kendziorek , Magdalena Lebiedzinska-Arciszewska , Mariusz R. Wieckowski , Justyna Janikiewicz , Agnieszka Dobrzyn

{"title":"Metformin promotes lipid droplet-mitochondria coupling and improves insulin secretion in pancreatic β-cells exposed to lipotoxicity","authors":"Aneta M. Dobosz , Ewelina Krogulec , Nataniel Stefanowski , Maria Kendziorek , Magdalena Lebiedzinska-Arciszewska , Mariusz R. Wieckowski , Justyna Janikiewicz , Agnieszka Dobrzyn","doi":"10.1016/j.bbalip.2025.159664","DOIUrl":"10.1016/j.bbalip.2025.159664","url":null,"abstract":"<div><div>Lipotoxicity that is caused by excess lipid accumulation is a major factor that contributes to gradual impairments of β-cell function and the development of type 2 diabetes. Metformin has shown protective effects against lipid-induced damage in β-cells, but its specific mechanisms of action within pancreatic islets remain unclear. The present study comprehensively examined direct effects of metformin on lipid metabolism pathways in INS-1E β-cells that were exposed to lipotoxic stress. Our results showed that metformin reduced both the number and size of lipid droplets in palmitate-treated INS-1E cells. This was followed by an increase in fatty acid utilization and the enhanced association between mitochondria and lipid droplets. Under conditions of palmitate overexposure, metformin limited the activity of adipose triglyceride lipase and lipogenic regulators, such as stearoyl-CoA desaturase, and suppressed fatty acid uptake into cells. Additionally, metformin alleviated triglyceride and free fatty acid accumulation and partially reversed palmitate-induced impairments in insulin secretion in INS-1E cells that were subjected to lipotoxicity. Notably, this beneficial effect of metformin on insulin secretion in INS-1E cells exposed to lipotoxic stress was less pronounced when the balance between mitochondrial fusion and fission was disturbed. These findings provide additional mechanistic insights into pleiotropic effects of metformin and its role in regulating β-cell function.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159664"},"PeriodicalIF":3.9,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular mechanisms of cytochrome P450-derived epoxy-fatty acids neuroprotection 细胞色素p450衍生的环氧脂肪酸神经保护的分子机制。

IF 3.9 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-10 DOI: 10.1016/j.bbalip.2025.159663

Cynthia Navarro-Mabarak, Julio Morán

{"title":"Molecular mechanisms of cytochrome P450-derived epoxy-fatty acids neuroprotection","authors":"Cynthia Navarro-Mabarak, Julio Morán","doi":"10.1016/j.bbalip.2025.159663","DOIUrl":"10.1016/j.bbalip.2025.159663","url":null,"abstract":"<div><div>The epoxyeicosatrienoic acids (EETs) are metabolites that result from the oxidation of the arachidonic acid by cytochrome P450 (CYP) epoxygenases. EETs are known to exert anti-inflammatory, antioxidant, vasodilatory, pro-angiogenic and anti-apoptotic actions. In the nervous system, EETs have been found to be neuroprotective in different models of neuronal damage. However, the molecular mechanisms responsible for these effects are not yet fully understood. This article seeks to review what is known about the signaling pathways involved in the EETs mediated neuroprotection. The mechanisms responsible for these effects are complex and involve several biological pathways that often crosstalk, including an inhibition of NFκB pathway, the activation of PPARα/γ nuclear receptors, and the activation of the PI3K/Akt pathway, among others. We also review what is known about the production and the biological significance of the epoxyeicosatrienoic acid ethanolamides (EET-EAs) and the epoxyeicosatrienoic acid glycerols (EET-EGs), metabolites that result from the epoxidation of the anandamide (AEA) and 2-arachidonylglycerol (2-AG) by CYP epoxygenases, which show endocannabinoid features.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159663"},"PeriodicalIF":3.9,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fatty acid binding protein 1 (FABP1) depletion promotes an oxidative metabolic shift in Caco-2 colorectal cancer cells 脂肪酸结合蛋白1 （FABP1）的缺失促进Caco-2结直肠癌细胞的氧化代谢转变。

IF 3.3 2区生物学

Biochimica et biophysica acta. Molecular and cell biology of lipids Pub Date : 2025-07-08 DOI: 10.1016/j.bbalip.2025.159661

Delfina Lucía Borús , Giorgia Zadra , Daniel Minsky , María Lucía Costa , Betina Córsico , Judith Storch , Natalia Scaglia

{"title":"Fatty acid binding protein 1 (FABP1) depletion promotes an oxidative metabolic shift in Caco-2 colorectal cancer cells","authors":"Delfina Lucía Borús , Giorgia Zadra , Daniel Minsky , María Lucía Costa , Betina Córsico , Judith Storch , Natalia Scaglia","doi":"10.1016/j.bbalip.2025.159661","DOIUrl":"10.1016/j.bbalip.2025.159661","url":null,"abstract":"<div><div>Lipid metabolism reprogramming is a well-established hallmark of many cancer types, including colorectal cancer (CRC). Nevertheless, a clear understanding on how fatty acid (FA) metabolism is fine-tuned during CRC development and progression is still missing. Given that CRC is the second leading cause of cancer-related death, addressing these critical aspects may provide the rationale for new therapeutic approaches and early biomarker identification. Fatty acid binding protein 1 (FABP1) is a small protein that binds FA and other lipophilic compounds, acting as a lipid transporter in the intestine. Little is currently known about the function of FABP1 in CRC. Here we show that the <em>knockdown</em> of FABP1 in CRC cells impairs <em>de novo</em> FA and cholesterol synthesis, specifically, <em>via</em> altering the transcriptional regulation of lipid metabolism genes. FABP1 depletion suppresses the expression of FA and cholesterol synthesis-associated genes while promoting that of FA oxidation genes and mitochondrial oxidative pathways. The latter is associated with increased oxygen consumption rate and activation of the energy sensor 5’ AMP-activated kinase (AMPK). Taken together, our results show that FABP1 orchestrates the balance between FA synthesis and oxidation, most likely to prevent the cytotoxic effects of circulating unbound free fatty acids. Thus, targeting FABP1 function may represent a potential therapeutic strategy in advanced CRC.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1870 7","pages":"Article 159661"},"PeriodicalIF":3.3,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0