Journal of Lipid Research最新文献

{"title":"Divergent effects of monomethyl branched-chain fatty acids on energy metabolism and insulin signaling in human myotubes.","authors":"Parmeshwar Bajirao Katare, Ragna H Tingstad, Sivar T Beajani, Jørgen Pasjkurov Indseth, Vibeke H Telle-Hansen, Mari C W Myhrstad, Arild C Rustan, Lars Eide, Oliwia Witczak, Vigdis Aas","doi":"10.1016/j.jlr.2025.100764","DOIUrl":"10.1016/j.jlr.2025.100764","url":null,"abstract":"<p><p>Branched-chain fatty acids (BCFAs) are predominantly saturated fatty acids with one or more methyl branches on the carbon chain, typically found in dairy products and measured in micromolar concentrations in human plasma. The biological function of BCFAs in humans remains ill-defined, but a relationship between circulating BCFAs and cardiometabolic health has been suggested. The objective of this study was to evaluate the impact of BCFAs on energy metabolism in human myotubes. The results revealed distinct effects of BCFAs. 12-Methyltetradecanoic acid (12-MTD) increased glucose uptake and glycogen synthesis, while 13-methyltetradecanoic acid (13-MTD), 14-methylhexadecanoic acid (14-MHD), and 15-methylhexadecanoic acid (15-MHD) increased oleic acid uptake and 13-MTD and 15-MHD oleic acid oxidation, indicating a more general stimulatory effect on fatty acid than glucose metabolism. Interestingly, the same BCFAs, 13-MTD, 14-MHD, and 15-MHD, appeared to reduce insulin-stimulated glycogen synthesis. Insulin-stimulated phosphorylation of IRS1 was not apparent after exposure to 12-MTD, 13-MTD, and 15-MHD, whereas insulin-stimulated phosphorylation of Akt was unchanged by BCFAs. Incorporation of [¹⁴C]leucine into lipids was affected, as 13-MTD increased the total lipid content, and 12-MTD altered the distribution of lipid classes. Metabolic flux analysis indicated that 14-MHD stimulated extracellular acidification. The effects of BCFAs might involve increased mRNA expression of pyruvate dehydrogenase kinase 4. In conclusion, the study demonstrates that different BCFAs have distinct effects on energy metabolism in myotubes, 12-MTD mainly affect glucose metabolism, while 13-MTD, 14-MHD, and 15-MHD modulated oleic acid metabolism. These data suggest that some BCFAs might have therapeutic applications by improving energy metabolism.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100764"},"PeriodicalIF":5.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143515888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional characterization of TMEM86A and TMEM86B mutants by a novel lysoplasmalogenase assay.","authors":"Denise Kummer, Ilaria Dorigatti, Theresia Dunzendorfer-Matt, Georg Golderer, Ernst R Werner, Katrin Watschinger","doi":"10.1016/j.jlr.2025.100766","DOIUrl":"10.1016/j.jlr.2025.100766","url":null,"abstract":"<p><p>Plasmalogens are an abundant class of glycero-phospholipids with a characteristic 1-O-alk-1'-enyl double bond. While their synthesis has been extensively investigated, their degradation remains understudied. Plasmalogen deficiencies are associated with severe disorders in humans and interfering with their degradation would be a treatment option, but it remains out of reach due to limited knowledge. The plasmalogen double bond is degraded either directly by a plasmalogenase or by conversion to the 2' lyso forms by phospholipase and subsequent cleavage by lysoplasmalogenase (E.C. 3.3.2.2). Two lysoplasmalogenases are known so far, TMEM86A and TMEM86B. While TMEM86B has been expressed in bacteria, purified, and shown to encode lysoplasmalogenase activity by a coupled optical assay, the closely related protein TMEM86A has not yet been purified, but its activity was shown indirectly by a lipidomics approach. Here, we present a novel assay for lysoplasmalogenase activity based on incubation with lysoplasmenylethanolamine or lysoplasmenylcholine, derivatization of the aldehyde product with dansylhydrazine, and hydrazone quantification by reversed-phase HPLC with fluorescence detection. The method was sensitive enough to robustly detect lysoplasmalogenase activity in human embryonic kidney cells following transient expression of TMEM86A or TMEM86B and also suitable for the determination of lysoplasmalogenase activity in mouse tissues where highest activities were found in liver and duodenum. We introduced point mutations at positions proposed to be catalytically relevant and provided experimental evidence that all but one affected lysoplasmalogenase activity. Our novel assay allows direct and fast measurement of lysoplasmalogenase activity, thereby providing a tool to advance research in the field of plasmalogen degradation.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100766"},"PeriodicalIF":5.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Do physiological changes in fatty acid composition alter cellular ferroptosis susceptibility and influence cell function?","authors":"Graeme I Lancaster, Andrew J Murphy","doi":"10.1016/j.jlr.2025.100765","DOIUrl":"10.1016/j.jlr.2025.100765","url":null,"abstract":"<p><p>Ferroptosis is an iron-dependent form of cell death driven by the excessive peroxidation of poly-unsaturated fatty acids (PUFAs) within membrane phospholipids. Ferroptosis is a hallmark of many diseases and preventing or inducing ferroptosis has considerable therapeutic potential. Like other forms of cell death, the pathological importance and therapeutic potential of ferroptosis is well appreciated. However, while cell death modalities such as apoptosis and necroptosis have critical physiological roles, such as in development and tissue homeostasis, whether ferroptosis has important physiological roles is largely unknown. In this regard, key questions for field are as follows: Is ferroptosis used for physiological processes? Are certain cell-types purposely adapted to be either resistant or sensitive to ferroptosis to be able to function optimally? Do physiological perturbations such as aging and diet impact ferroptosis susceptibility? Herein, we have reviewed emerging evidence that supports the idea that being able to selectively and controllably induce or resist ferroptosis is essential for development and cell function. While several factors regulate ferroptosis, it appears that the ability of cells and tissues to control their lipid composition, specifically the abundance of phospholipids containing PUFAs, is crucial for cells to be able to either resist or be sensitized to ferroptosis. Finally, aging and diets enriched in specific PUFAs lead to an increase in cellular PUFA levels which may sensitize cells to ferroptosis. Therefore, changes in dietary PUFAs or againg may impact the pathogenesis of diseases where ferroptosis is involved.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100765"},"PeriodicalIF":5.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Foamy monocytes and atherogenesis in mice with combined hyperlipidemia and effects of antisense knockdown of apoCIII.","authors":"Xueying Peng, Zeqin Lian, Veronica O'Brien, Jing Xiao, Benjamin A Litchfield, Xiao-Yuan Dai Perrard, Lu Xu, Jing Ni, Aparna Mukherjee, Timothy Simmons, Henry Dong, Adam E Mullick, Rosanne Crooke, Henry J Pownall, Scott I Simon, Christie M Ballantyne, Huaizhu Wu","doi":"10.1016/j.jlr.2025.100763","DOIUrl":"10.1016/j.jlr.2025.100763","url":null,"abstract":"<p><p>Hypertriglyceridemia (HTG), particularly in combined hyperlipidemia, increases risk for atherosclerotic cardiovascular disease, but the underlying mechanisms remain incompletely understood. We sought to determine contributions of circulating monocytes to atherosclerosis associated with HTG in combined hyperlipidemia, created by transgenic expression of human apoCIII in Ldlr^-/- mice (Ldlr^-/-ApoCIIItg) fed Western high-fat diet (WD). Tissue culture with THP-1 and primary human monocytes was used to examine effects of triglyceride (TG)-rich lipoproteins on monocytes. Ldlr^-/-ApoCIIItg mice were also treated with apoCIII antisense oligonucleotide (ASO) and examined for foamy monocytes and atherosclerosis. Compared to Ldlr^-/- mice, Ldlr^-/-ApoCIIItg mice fed WD had early and persistent increases in lipid accumulation within monocytes and enhanced atherosclerosis. Ldlr^-/-ApoCIIItg mice versus Ldlr^-/- mice had higher levels of CD11c, CD36, and cytokines in foamy monocytes, with increases in foamy monocyte adhesion to vascular cell adhesion molecule-1 and oxidized LDL uptake. Monocytes took up TG-rich lipoprotein in vivo and in vitro and changed phenotypes. Foamy monocytes infiltrated into atherosclerotic lesions, and specific and sustained depletion of CD11c⁺ (foamy) monocytes profoundly reduced atherosclerosis in Ldlr^-/-ApoCIIItg mice on WD. Treatment with apoCIII ASO lowered plasma TG and cholesterol levels, improved foamy monocyte phenotypes, and reduced atherosclerosis in Ldlr^-/-ApoCIIItg mice. In conclusion, HTG in combined hyperlipidemia accelerates atherosclerosis, in part, by increasing foamy monocyte formation and infiltration into atherosclerotic plaques. Treatment with apoCIII ASO is a potential new therapy for improving monocyte phenotypes and reducing atherosclerosis in combined hyperlipidemia.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100763"},"PeriodicalIF":5.0,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taurine alleviates dysfunction of cholesterol metabolism under hyperuricemia by inhibiting A2AR-SREBP-2/CREB/HMGCR axis.","authors":"Beibei Chen, Ruixia Bao, Jujie Pan, Zicheng Zhu, Qian Chen, Dan Wang, Yuzheng Wu, Haiyang Yu, Yi Zhang, Tao Wang","doi":"10.1016/j.jlr.2025.100746","DOIUrl":"10.1016/j.jlr.2025.100746","url":null,"abstract":"<p><p>Dysfunctional cholesterol metabolism is highly prevalent in patients with hyperuricemia. Both uric acid and cholesterol are independent risk factors for atherosclerosis, contributing to an increased incidence of cardiovascular disease in hyperuricemia. Investigating the pathological mechanisms underlying cholesterol metabolism dysfunction in hyperuricemia is essential. This study identified adenosine and inosine, two major purine metabolites, as key regulators of cholesterol biosynthesis. These metabolites upregulate 3-hydroxy-3-methylglutaryl-CoA. Further mechanistic studies revealed that adenosine/inosine up-regulated the expression of 3-hydroxy-3-methylglutaryl-CoA by activating adenosine A2A receptor via the Srebp-2/Creb axis in hyperuricemia. Additionally, we found that taurine deficiency contributes to cholesterol metabolism dysfunction in hyperuricemia. Taurine administration in hyperuricemia mice significantly reduced cholesterol elevation by inhibiting adenosine A2A receptor. This study provides a promising strategy for treating comorbid hypercholesterolemia and hyperuricemia.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100746"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiological accumulation of lipid droplets in the newborn liver during breastfeeding is driven by TLR4 ligands.","authors":"Wanderson Ferreira da Silva Júnior, Karen Marques de Oliveira Costa, Hortência Maciel Castro Oliveira, Maísa Mota Antunes, Kassiana Mafra, Brenda Naemi Nakagaki, Pedro Sérgio Corradi da Silva, Júlia Duarte Megale, Sarah Campos de Sales, Douglas Carvalho Caixeta, Mário Machado Martins, Robinson Sabino-Silva, Cristina Maria Pinto de Paula, Luiz Ricardo Goulart, Rafael Machado Rezende, Gustavo Batista Menezes","doi":"10.1016/j.jlr.2025.100744","DOIUrl":"10.1016/j.jlr.2025.100744","url":null,"abstract":"<p><p>The liver plays a central role in fat storage, but little is known about physiological fat accumulation during early development. Here we investigated a transient surge in hepatic lipid droplets observed in newborn mice immediately after birth. We developed a novel model to quantify liver fat content without tissue processing. Using high-resolution microscopy assessed the spatial distribution of lipid droplets within hepatocytes. Lugol's iodine staining determined the timing weaning period, and milk deprivation experiments investigated the relationship between milk intake and fat accumulation. Lipidomic analysis revealed changes in the metabolic profile of the developing liver. Finally, we investigated the role of Toll-like receptor 4 (TLR4) signaling in fat storage using knockout mice and cell-specific deletion strategies. Newborn mice displayed a dramatic accumulation of hepatic lipid droplets within the first 12 h after birth, persisting for the initial two weeks of life. This pattern coincided with exclusive milk feeding and completely abated by the third week, aligning with weaning. Importantly, the observed fat accumulation shared characteristics with established models of pathological steatosis, suggesting potential biological relevance. Lipid droplets were primarily localized within the cytoplasm of hepatocytes. Milk deprivation experiments demonstrated that milk intake is the primary driver of this transient fat accumulation. Lipidomic analysis revealed significant changes in the metabolic profile of newborn livers compared to adults. Interestingly, several highly abundant lipids in newborns were identified as putative ligands for TLR4. Subsequent studies using TLR4-deficient mice and cell-specific deletion revealed that TLR4 signaling, particularly within hepatocytes, plays a critical role in driving fat storage within the newborn liver. Additionally, a potential collaboration between metabolic and immune systems was suggested by the observed effects of myeloid cell-specific TLR4 ablation. This study demonstrates a unique phenomenon of transient hepatic fat accumulation in newborn mice driven by milk intake and potentially regulated by TLR4 signaling, particularly within hepatocytes.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100744"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contribution of individual phospholipase A₂ enzymes to the cleavage of oxidized phospholipids in human blood plasma.","authors":"Philipp Jokesch, Olga Oskolkova, Maria Fedorova, Bernd Gesslbauer, Valery Bochkov","doi":"10.1016/j.jlr.2025.100742","DOIUrl":"10.1016/j.jlr.2025.100742","url":null,"abstract":"<p><p>Phospholipids containing oxidized esterified PUFA residues (OxPLs) are increasingly recognized for multiple biological activities and causative involvement in disease pathogenesis. Pharmacokinetics of these compounds in blood plasma is essentially not studied. Human plasma contains both genuine phospholipases A₂ [platelet activating factor acetyl hydrolase (PAF-AH) (also called Lp-PLA₂) and secretory phospholipase A2] and multifunctional enzymes capable of removing sn-2 residues in native and oxidized PLs (lecithin-cholesterol acyltransferase, peroxiredoxin-6). The goal of this study was to compare relative activities of different PLA₂ enzymes by analyzing cleavage of oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylcholine (OxPAPC) and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylethanolamine (OxPAPE) by diluted plasma in the presence of enzyme inhibitors. We have found that human plasma demonstrated high total PLA₂ activity against oxidized PCs and PEs. PAF-AH/Lp-PLA₂ played a dominant role in LysoPC and LysoPE production as compared to other enzymes. Molecular species of oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylcholine and oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphatidylethanolamine could be divided into three groups according to their degradation rate and sensitivity to PAF-AH/Lp-PLA₂ inhibitor darapladib. Oxidatively truncated species were most rapidly metabolized in the presence of plasma; this process was strongly inhibited by darapladib. The rate of degradation of full-length OxPLs depended on the degree of oxygenation. Species containing 1 to 3 oxygen atoms were relatively stable to degradation in plasma, while OxPLs containing > 3 extra oxygens were degraded but at significantly slower rate than truncated species. In contrast to truncated species, degradation of full-length OxPLs with > 3 extra oxygens were only minimally inhibited by darapladib. These data provide further insights into the mechanisms regulating circulating levels of OxPLs and lipid mediators generated by PLA₂ cleavage of OxPLs, namely oxylipins and LysoPC.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100742"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11841071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142950238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Competitive displacement of lipoprotein lipase from heparan sulfate is orchestrated by a disordered acidic cluster in GPIHBP1.","authors":"Anamika Biswas, Samina Arshid, Kristian Kølby Kristensen, Thomas J D Jørgensen, Michael Ploug","doi":"10.1016/j.jlr.2025.100745","DOIUrl":"10.1016/j.jlr.2025.100745","url":null,"abstract":"<p><p>Movement of lipoprotein lipase (LPL) from myocytes or adipocytes to the capillary lumen is essential for intravascular lipolysis and plasma triglyceride homeostasis-low LPL activity in the capillary lumen causes hypertriglyceridemia. The trans-endothelial transport of LPL depends on ionic interactions with GPIHBP1's intrinsically disordered N-terminal tail, which harbors two acidic clusters at positions 5-12 and 19-30. This polyanionic tail provides a molecular switch that controls LPL detachment from heparan sulfate proteoglycans (HSPGs) by competitive displacement. When the acidic tail was neutralized in gene-edited mice, LPL remained trapped in the sub-endothelial spaces triggering hypertriglyceridemia. Due to its disordered state, the crystal structure of LPL•GPIHBP1 provided no information on these electrostatic interactions between LPL and GPIHBP1 acidic tail. In the current study, we positioned the acidic tail on LPL using zero-length crosslinking. Acidic residues at positions 19-30 in GPIHBP1 mapped to Lys⁴⁴⁵, Lys⁴⁴¹, Lys⁴¹⁴, and Lys⁴⁰⁷ close to the interface between the C- and N-terminal domains in LPL. Modeling this interface revealed widespread polyelectrolyte interactions spanning both LPL domains, which explains why the acidic tail stabilizes LPL activity and protein conformation. In functional assays, we showed that the acidic cluster at 19-30 also had the greatest impact on preserving LPL activity, mitigating ANGPTL4-catalyzed LPL inactivation, preventing PSCK3-mediated LPL cleavage, and, importantly, displacing LPL from HSPGs. Our current study provides key insights into the biophysical mechanism(s) orchestrating intravascular compartmentalization of LPL activity-an intriguing pathway entailing competitive displacement of HSPG-bound LPL by a disordered acidic tail in GPIHBP1.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100745"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11869522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Participation of lipids in the tumor response to photodynamic therapy and its exploitation for therapeutic gain.","authors":"Mladen Korbelik, Michal Heger, Albert W Girotti","doi":"10.1016/j.jlr.2024.100729","DOIUrl":"10.1016/j.jlr.2024.100729","url":null,"abstract":"<p><p>Hydroperoxides of unsaturated membrane lipids (LOOHs) are the most abundant non-radical intermediates generated by photodynamic therapy (PDT) of soft tissues such as tumors and have far longer average lifetimes than singlet oxygen or oxygen radicals formed during initial photodynamic action. LOOH-initiated post-irradiation damage to remaining membrane lipids (chain peroxidation) or to membrane-associated proteins remains largely unrecognized. Such after-light processes could occur during clinical oncological PDT, but this is not well-perceived by practitioners of this therapy. In general, the pivotal influence of lipids in tumor responses to PDT needs to be better appreciated. Of related importance is the fact that most malignant tumors have dramatically different lipid metabolism compared with healthy tissues, and this too is often ignored. The response of tumors to PDT appears especially vulnerable to manipulations within the tumor lipid microenvironment. This can be exploited for therapeutic gain with PDT, as exemplified here by the combined treatment with the antitumor lipid edelfosine.</p>","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100729"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911859/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Staying sane in the membrane: Neutral sphingomyelinase 2 as a master regulator of plasma membrane ceramide.","authors":"Zainuddin Quadri, Erhard Bieberich","doi":"10.1016/j.jlr.2024.100737","DOIUrl":"10.1016/j.jlr.2024.100737","url":null,"abstract":"","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100737"},"PeriodicalIF":5.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142895343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}