Biochimica et biophysica acta. Molecular and cell biology of lipids最新文献

{"title":"A sweet potato vine-derived peptide ST2b alleviates type 2 diabetes via stabilizing INSIG-1 to inhibit SREBP-2-driven lipotoxicity.","authors":"Menglei Chen, Jing Chen, Ke Liu, Xinxin Zhang, Yipeng Sun, Yige Fang, Bo Yuan, Jiebang Jiang, Rongpeng Li, Fei Wang","doi":"10.1016/j.bbalip.2026.159770","DOIUrl":"10.1016/j.bbalip.2026.159770","url":null,"abstract":"<p><p>Sterol Regulatory Element-Binding Protein 2 (SREBP-2) is a core transcription factor that regulates de novo cholesterol synthesis. Targeting the SREBP pathway is regarded as a potential strategy for treating metabolic diseases such as Type 2 Diabetes Mellitus (T2DM). At present, natural specific and effective modulators of this pathway are still very scarce. We identified a novel nonapeptide ST2b from the vine of the medicinal sweet potato Ipomoea batatas L. cv. Simon 1, and its amino acid sequence is GSFKMEGKR. In vitro experiments have shown that ST2b can significantly promote glucose uptake in insulin-resistant HepG2 cells and improve disorders of glycolipid metabolism. In a mouse model of T2DM induced by streptozotocin and a high-fat, high-sugar diet, intragastric ST2b reduced fasting blood glucose and serum insulin levels, improved glucose tolerance and insulin sensitivity, normalized lipid metabolism, and protected metabolic organs. ST2b binds to INSIG-1, stabilizing it by inhibiting degradation, enhancing INSIG-1 interaction with SCAP, blocking SREBP-2 activation, reducing cholesterol synthesis gene transcription. ST2b from sweet potatoes shows promise as a T2DM treatment by inhibiting the SREBP-2 pathway, suggesting its potential as a therapeutic agent or functional food for T2DM.</p>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":" ","pages":"159770"},"PeriodicalIF":3.8,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879072","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}

{"title":"Astaxanthin attenuates pro-inflammatory signaling and promotes adipogenesis in human adipose stem cells.","authors":"Fiorenzo Toncan, Yuka Yamamoto, Radha Raman Raj, Madhu Bharti, Mi-Jeong Lee","doi":"10.1016/j.bbalip.2026.159769","DOIUrl":"https://doi.org/10.1016/j.bbalip.2026.159769","url":null,"abstract":"<p><p>Adipose tissues not only store and release energy but also function as endocrine organs and maintaining adipose stem cells (ASCs) and functional adipocytes is essential for systemic metabolic health. Astaxanthin (Ast), an oxygenated carotenoid enriched in seafood, is recognized as a bioactive compound known for its anti-inflammatory and antioxidative properties. However, limited information is available regarding the roles of Ast in human ASCs (hASCs). This study examined the capacity of Ast to counteract TNF-α actions in the inflammatory signaling pathways and proliferation of hASCs. The effects of Ast on hASC adipogenesis and the underlying mechanisms were also determined. Proliferation rates were measured with an MTT assay, and adipogenesis was determined by measuring the expression levels of adipogenic markers and lipid accumulation. Ast (0.01-10 μM) had no effect under basal conditions but attenuated TNFα-mediated suppression of cell viability, as well as activation of canonical proinflammatory signaling pathways in hASCs. Lower concentrations of Ast (0.01 and 0.1 μM) increased adipogenesis, while higher concentrations (2 and 10 μM) inhibited adipogenesis. Ast (0.01 and 0.1 μM) induced adipogenesis by suppressing the anti-adipogenic Wnt/β-catenin pathway and upregulating the adipogenic transcription factors, C/EBPα and PPARγ, during the early periods of adipogenesis. Our results suggest that Ast has beneficial impacts on adipose tissue by suppressing inflammation, thereby maintaining the pool of adipose progenitors and promoting their adipogenesis.</p>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":" ","pages":"159769"},"PeriodicalIF":3.8,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863463","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}

{"title":"Attenuation of liver fibrosis by platelet-type 12S-lipoxygenase expressed in hepatic stellate cells involves repression of platelet-derived growth factor receptors.","authors":"Keisuke Toda, Rena Tamai, Ryoma Tanaka, Nanomi Araki, Maho Ishihara, Hibiki Kanji, Izumi Tsukayama, Yuki Kawakami, Toshiko Suzuki-Yamamoto, Yoshitaka Takahashi","doi":"10.1016/j.bbalip.2026.159768","DOIUrl":"10.1016/j.bbalip.2026.159768","url":null,"abstract":"<p><p>Progression of liver fibrosis is a critical determinant of the prognosis of chronic inflammatory liver disease. We previously reported that platelet-type 12S-lipoxygenase localized in hepatic stellate cells (HSCs), which are primary fibrogenic cells in the injured liver, was upregulated in a methionine-choline deficiency (MCD) diet-induced mouse liver fibrosis model. In this study, the functional contribution of platelet-type 12S-lipoxygenase to the pathological process was investigated. After feeding with an MCD diet for 8 weeks, platelet-type 12S-lipoxygenase-deficient (Alox12^-/-) mice exhibited significantly greater Sirius Red-positive areas and higher expression of type I collagen genes (Col1a1 and Col1a2) than wild-type (WT) mice, indicating aggravated fibrosis. Similar results were obtained in a model induced by neonatal streptozotocin injection followed by a high-fat diet (HFD) feeding. Conversely, a human HSC line (TWNT-1) stably overexpressing human platelet-type 12S-lipoxygenase exhibited significantly reduced COL1A1 and COL1A2 expression compared to the parental and mock cells. Analysis of fibrosis-related genes revealed downregulation of platelet-derived growth factor receptors (PDGFR) α and β in platelet-type 12S-lipoxygenase-expressing TWNT-1 cells. Consistently, the hepatic expression of Pdgfra and Pdgfrb was significantly elevated in MCD diet-fed Alox12^-/- mice compared to that in MCD diet-fed WT mice. The knockdown of PDGFRs in parental TWNT-1 cells using siRNAs significantly suppressed the expression of type I collagen genes. Collectively, these findings indicate that platelet-type 12S-lipoxygenase expressed in HSCs attenuates liver fibrosis, at least in part, by modulating PDGFR expression.</p>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":" ","pages":"159768"},"PeriodicalIF":3.8,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148838660","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}

{"title":"Role of lipid droplet-mediated lipid peroxidation by GPX4 in docosahexaenoic acid-induced EA.hy926 endothelial cell ferroptosis","authors":"Youjia Du ,&nbsp;Yan Shen ,&nbsp;Ruotong Wang ,&nbsp;Xiaoou Ren ,&nbsp;Shoudong Ye","doi":"10.1016/j.bbalip.2026.159748","DOIUrl":"10.1016/j.bbalip.2026.159748","url":null,"abstract":"<div><div>Endothelial cells (EC) form the inner lining of the blood vessels and are essential for the vascular homeostasis. EC death has been implicated in the pathology of vascular diseases. Our previous studies indicated that docosahexaenoic acid (DHA) induces EA.hy926 EC death by upregulating lipid droplet (LD) biogenesis and activating p38 MAPK, however, how LDs contribute to this process remains unclear. DHA belongs to the polyunsaturated fatty acids that are susceptible to lipid peroxidation, which is a common mechanism in lipid-induced cell injury and ferroptosis. Therefore, the current study is to investigate the mechanism of LD in the regulation of lipid peroxidation in relation to p38 MAPK in DHA-induced EA.hy926 endothelial ferroptosis. Results showed that DHA induced a time-dependent, bidirectional modulation of GPX4 expression accompanied by a progressive GSH and NADPH depletion and increased lipid peroxidation in ECs. Suppression of LD formation through diacylglycerol acyltransferases inhibition, siRNA, or promotion of LD lipolysis reduced lipid peroxidation and restored the GPX4 expression. Inhibiting lipid peroxidation chemically, activating GPX4 or supplementing GSH all prevented the cell death by DHA. Our findings reveal a novel role of LD in regulating GPX4-mediated lipid peroxidation and highlight the key role of p38 MAPK in downregulating GPX4 in lipid peroxidation-induced EC ferroptosis by DHA. In conclusion, the present study suggested that DHA-induced LD formation in ECs increases the membrane area, which could facilitate the lipid peroxidation reaction, disrupt the endogenous GPX4 antioxidant system, and thereby exacerbate the detrimental effects of lipid peroxidation, ultimately leading to cell ferroptosis.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 5","pages":"Article 159748"},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052260","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}

{"title":"Spatial gradients of lipase activity govern lipid droplet remodeling in the zebrafish embryo","authors":"Sudipta Sarkar ,&nbsp;Sayani Haldar ,&nbsp;Subhasis Mandal ,&nbsp;Nandana Nanda ,&nbsp;Subrata Karmakar ,&nbsp;Prosenjit Sen ,&nbsp;Deepak Kumar Sinha","doi":"10.1016/j.bbalip.2026.159747","DOIUrl":"10.1016/j.bbalip.2026.159747","url":null,"abstract":"<div><div>Early zebrafish embryos rely on maternally supplied yolk lipids to fuel growth before the onset of feeding; yet, how these lipids are mobilized and redistributed remains poorly understood. Here, we combine live imaging with the solvatochromic dye Nile Red to map lipid composition in space and time through changes in the emission peak, a readout of local polarity. We show that lipid droplets (LDs) in the blastodisc are highly heterogeneous in size and polarity at the “one-cell stage” but progressively homogenize as development proceeds. LDs originate at the yolk–blastodisc interface, where localized lipase activity drives their biogenesis and initial composition. As LDs migrate toward the animal pole, their polarity increases, reflecting continuous lipolysis within a spatially confined metabolic zone. Smaller LDs display greater lipolytic efficiency than larger ones, linking droplet geometry to metabolic turnover. Inhibition of lipase activity disrupts both LD formation and lipid cycling, demonstrating that shared enzymatic machinery underlies droplet synthesis and degradation. Together, our findings reveal a spatially organized and developmentally regulated lipid metabolism in the zebrafish blastodisc, where local enzyme activity, droplet mechanics, and lipid composition are dynamically coupled. This live-imaging approach establishes a framework for studying lipid regulation in vertebrate development and disease.</div></div><div><h3>Digest summary</h3><div>By visualizing lipids in living zebrafish embryos, this study reveals that lipid droplets are not passive fat stores but dynamic organelles whose size, composition, and behavior are shaped by local enzyme activity at the yolk–blastodisc interface, offering new insight into how developing cells control their energy reserves.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 5","pages":"Article 159747"},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148026392","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}

{"title":"Maximization of mitochondrial fatty acid oxidation by co-administration of PPARα agonist and peroxisomal β-oxidation inhibitor","authors":"Ziyu Zeng ,&nbsp;Yicong Li ,&nbsp;Junwei Cao ,&nbsp;Wei Zhang,&nbsp;Yida Zhang,&nbsp;Haoya Yao,&nbsp;Yaoqing Wang,&nbsp;Jia Zeng","doi":"10.1016/j.bbalip.2026.159750","DOIUrl":"10.1016/j.bbalip.2026.159750","url":null,"abstract":"<div><div>PPARα plays a pivotal role in regulating hepatic fatty acid oxidation and activation of PPARα has been well known to stimulate mitochondrial β-oxidation and has the potential to reduce hepatic lipid level, while evidences indicate that administration of PPARα agonist does not affect hepatic triglyceride level. Therefore, an alternative mechanism might work to counteract the lipid-lowering effect of PPARα agonist. As fatty acids can also be metabolized in peroxisome and the acetyl-CoA generated in peroxisomal β-oxidation could be used for the biosynthesis of malonyl-CoA, a critical molecule in controlling mitochondria fatty acid oxidation. We hypothesize that peroxisomal β-oxidation might play a role in regulating mitochondrial fatty acid oxidation through mediating malonyl-CoA formation. This study demonstrates a counteracting mechanism by which induction of peroxisomal β-oxidation causes suppression of mitochondrial fatty acid oxidation in animals administered with PPARα agonist. PPARα agonist induces oxidation of fatty acids by peroxisomes and generates considerable acetate in the liver, which significantly elevates hepatic content of malonyl-CoA, and causes suppression of mitochondrial β-oxidation. Specific inhibition of peroxisomal β-oxidation enhances mitochondrial fatty acid oxidation and attenuates hepatic lipid accumulation by reducing acetate and malonyl-CoA formation in the mice treated with PPARα agonist. It is suggested that combination therapy of PPARα agonist and peroxisomal β-oxidation inhibitor might be a novel and effective treatment of fatty liver and related metabolic disorder through maximization of mitochondrial fatty acid oxidation.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 5","pages":"Article 159750"},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052218","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}

{"title":"Enhydrin from yacon attenuates atherosclerosis by modulating the FABP5/PPARγ/ABCA1 axis: An integrated multi-omics and in vivo validation","authors":"Chao Tian ,&nbsp;Guiping He ,&nbsp;Ling Zu ,&nbsp;Chaoqun Bi ,&nbsp;Zunqiu Wu ,&nbsp;Jianfei Sun","doi":"10.1016/j.bbalip.2026.159751","DOIUrl":"10.1016/j.bbalip.2026.159751","url":null,"abstract":"<div><div>Dysregulated lipid metabolism drives atherosclerosis (AS). Yacon, an Andean lipid-modulating tuber, exerts anti-AS potential, but mechanisms remain unclear. We integrated network pharmacology, machine learning, single-cell RNA sequencing (scRNA-seq), and in vivo validation to explore its anti-AS effects and targets. Active constituents and targets were curated from literature, TCMSP, and SwissTargetPrediction; lipid/AS genes from GeneCards, OMIM, and GEO were filtered via limma, WGCNA, LASSO, randomForest, and SVM-RFE. Immune infiltration and external validation confirmed hub gene relevance. scRNA-seq prioritized FABP5; docking and dynamics quantified compound–FABP5 interactions. In vivo efficacy was tested in high-fat diet (HFD)-fed ApoE−/− mice via histology (Oil Red O, H&amp;E, and Masson) and molecular assays (RT-qPCR, Western blot, and immunofluorescence). We identified 12 constituents, 384 targets, and seven core targets (AURKA, MMP9, FABP5, etc.), with FABP5 top-ranked. Docking and dynamics identified Enhydrin as the strongest FABP5 binder. Enhydrin administration was associated with reduced hepatic lipid accumulation, decreased serum triacylglycerol (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels, and increased high-density lipoprotein cholesterol (HDL<img>C) levels. Histopathological analysis of arterial tissues revealed attenuated vascular lipid deposition and delayed atherosclerotic lesion progression. Across assays, Enhydrin downregulated FABP5, reduced abnormal fatty acid trafficking, and upregulated PPARγ and ABCA1, with markedly reduced vascular lipid deposition and improved serum lipid profiles, reflecting enhanced cholesterol efflux. Conclusion: Our integrative multi-omics analysis pinpointed FABP5 as a promising novel target for yacon-derived Enhydrin in atherosclerosis. In vivo, Enhydrin markedly downregulated FABP5 and upregulated PPARγ and ABCA1, suggesting this axis mediates its anti-atherosclerotic activity.</div></div><div><h3>Significance statement</h3><div>1: This study identified FABP5 as a candidate target for atherosclerosis through integrative multi-omics, and its association with the anti-atherosclerotic effects of Enhydrin suggests therapeutic potential.</div><div>2: The anti-atherosclerotic effects of yacon's active components and their underlying molecular pathways were systematically screened and preliminarily characterized by integrating bioinformatic prediction with in vivo validation, laying a preliminary theoretical foundation for further pharmacological investigation and clinical translation.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 5","pages":"Article 159751"},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148100969","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}

{"title":"Gm15441 improves adipogenesis and insulin sensitivity by TXNIP regulation in white adipose tissue","authors":"Yinze Shi ,&nbsp;Liying Huang ,&nbsp;Xueyang Yang ,&nbsp;Jiaoyue Zhang ,&nbsp;Lulu Chen","doi":"10.1016/j.bbalip.2026.159718","DOIUrl":"10.1016/j.bbalip.2026.159718","url":null,"abstract":"<div><div><em>Gm15441</em>, a long non-coding RNA antisense to thioredoxin interacting protein (TXNIP) mRNA, exhibits undefined roles in adipogenesis and insulin resistance. This study aimed to explore its functions and mechanisms in white adipose tissue (WAT). <em>Gm15441</em> expression was assessed in 3T3-L1 cells and WAT of insulin-resistant mice. Stable <em>Gm15441</em> overexpression and knockdown 3T3-L1 cell models were established, followed by differentiation induction and analysis of lipid accumulation and differentiation markers. A subcutaneous adipose-specific <em>Gm15441</em> overexpression mouse model was fed high-fat diets (HFD) and evaluated for metabolic parameters, adipogenesis, and insulin signaling. Subcellular localization in vitro was determined via fluorescence in situ hybridization, while transcriptome sequencing, TXNIP expression analysis, and RNA-RNA pull-down assays were performed. Results showed that <em>Gm15441</em> expression increased during cell differentiation and decreased in insulin-resistant WAT. <em>Gm15441</em> overexpression promoted adipogenesis in vitro, while knockdown suppressed it. In HFD-fed mice, adipose-specific <em>Gm15441</em> overexpression enhanced adipogenesis, reduced blood glucose, and improved insulin sensitivity. Although PPARγ expression increased with cell differentiation, <em>Gm15441</em> probes did not pull down PPARγ mRNA. Conversely, TXNIP protein levels decreased in <em>Gm15441</em>-overexpressing cells without corresponding changes in mRNA levels, but <em>Gm15441</em> probes successfully pulled down TXNIP mRNA. These results suggested that <em>Gm15441</em> may promote adipogenesis and enhance insulin sensitivity by inhibiting TXNIP expression.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 3","pages":"Article 159718"},"PeriodicalIF":3.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965026","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}

{"title":"Substituents of the polysaccharide region of LPS in Legionella pneumophila sg1 modulate interactions with host cells","authors":"Bożena Kowalczyk ,&nbsp;Agnieszka Szuster-Ciesielska ,&nbsp;Zbigniew Kaczyński ,&nbsp;Markus Petzold ,&nbsp;Christina E. Galuska ,&nbsp;Beate Fuchs ,&nbsp;Rafal Luchowski ,&nbsp;Wiesław I. Gruszecki ,&nbsp;Piotr Koper ,&nbsp;Adam Choma ,&nbsp;Jacek Tarasiuk ,&nbsp;Marta Palusińska-Szysz","doi":"10.1016/j.bbalip.2026.159720","DOIUrl":"10.1016/j.bbalip.2026.159720","url":null,"abstract":"<div><div><em>Legionella pneumophila</em> is a Gram-negative bacterium commonly found in natural freshwater reservoirs, where it exists as an intracellular parasite of cohabiting protozoa, primarily of the genus <em>Acanthamoeba</em>. Inhalation of aerosol contaminated with the bacterium leads to its proliferation within pulmonary macrophages, ultimately resulting in pneumonia known as Legionnaires' disease. The lipopolysaccharide (LPS) of <em>L. pneumophila</em> sg1 constitutes the most exposed component of the bacterial cell wall, playing a key role in every stage of its developmental cycle associated with host cells. The <em>orf8</em> gene encodes an <em>N</em>-methyltransferase responsible for the methylation of the 5-acetimidoylamino group in legionaminic acid of LPS of <em>L. pneumophila</em> sg1 strain 130b. Mutants impaired in synthesizing <em>N</em>-methyl groups of legionaminic acid produce neutral lipids, sphingolipids, and ceramides with an altered composition compared to the wild-type strain. <em>N</em>-methyl groups in legionaminic acid enhance bacterial adhesion to <em>Acanthamoeba castellanii</em> cells and THP-1-derived macrophages. Their occurrence, however, reduces the adhesion capacity of <em>L. pneumophila</em> sg1 strain 130b to epithelial cells of the A549 and BEAS-2B lines.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 3","pages":"Article 159720"},"PeriodicalIF":3.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986713","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}

{"title":"Palmitoylated STX11 suppresses AMPK to drive lipogenesis and colorectal cancer","authors":"Bao Li ,&nbsp;Zhongkang Yan ,&nbsp;Wenyuan Dang ,&nbsp;Jianxiong Han ,&nbsp;Hongli Xue ,&nbsp;Feifei Wang ,&nbsp;Lili Wang ,&nbsp;Xueqing Yang ,&nbsp;Xingyuan Yang","doi":"10.1016/j.bbalip.2026.159730","DOIUrl":"10.1016/j.bbalip.2026.159730","url":null,"abstract":"<div><div>Syntaxin 11(STX11), a SNARE family protein, regulates vesicular trafficking and cytokinesis, yet its functional role in colorectal cancer (CRC) pathogenesis remains poorly understood. Here, we identify STX11 as a critical regulator that potentiates CRC progression in vivo and in vitro. Mechanistically, STX11 modulates the AMPK signaling pathway in a palmitoylation-dependent manner, attenuating ACC phosphorylation to enhance its enzymatic activity and stimulate de novo lipogenesis. Genetic ablation of STX11 significantly impedes tumorigenesis in an AOM/DSS-induced CRC mouse model. Our findings establish STX11 as a critical regulator of lipid metabolism in CRC progression and nominate it as a promising therapeutic target.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 3","pages":"Article 159730"},"PeriodicalIF":3.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099818","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}