Prostaglandins & other lipid mediators最新文献

{"title":"Role of IRGM in acute lung injury: Inducing mitophagy and inactivating cGAS-STING signaling to improve lipopolysaccharide-induced alveolar epithelial barrier dysfunction","authors":"Yanqiong Shi,&nbsp;Yang Liang,&nbsp;Yang Chen,&nbsp;Zhenghuan Li","doi":"10.1016/j.prostaglandins.2025.107026","DOIUrl":"10.1016/j.prostaglandins.2025.107026","url":null,"abstract":"<div><div>Acute lung injury (ALI) is a common disorder of the respiratory system with high mortality. Inducing mitophagy is generally considered to be an effective target for alleviating ALI. We aimed to elucidate the role of immunity related GTPase M (IRGM) in ALI by using a lipopolysaccharide (LPS)-induced alveolar epithelial cell model. Firstly, IRGM expression in A549 cells under LPS conditions was evaluated. Then, IRGM was upregulated and oxidative stress was evaluated by measuring intracellular reactive oxygen species (ROS) using 2′, 7′-Dichlorofluorescin diacetate (DCFH-DA) staining. The permeability of A549 cells was determined by detecting transepithelial electrical resistance (TEER) value and fluorescein isothiocyanate-dextran 4 (FITC-FD4) fluorescence. Proteins related to epithelial barrier, mitophagy and mitochondrial function were assessed. Further Mdivi-1 (an inhibitor of mitophagy) addition or cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling overexpression was conducted to investigate the potential mechanism. Results suggested that IRGM was downregulated in LPS-treated A549 cells and IRGM upregulation alleviated LPS-induced oxidative stress, inflammation and barrier dysfunction in A549 cells. IRGM upregulation induced mitophagy and maintains mitochondrial function in LPS-treated A549 cells. Particularly, Mdivi-1 treatment or cGAS overexpression abrogated the impacts of IRGM upregulation on oxidative stress, inflammation and barrier dysfunction in LPS-treated A549 cells. Collectively, IRGM attenuates LPS-triggered alveolar epithelial cell damage by enhancing mitophagy to inactivate cGAS/STING signaling.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107026"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic profiling of bioactive components from Schizophyllum commune Fries in hypercholesterolemic Wistar-Kyoto rats using LC-QTOF-MS analysis","authors":"Rushitha Sadasevevam,&nbsp;Norhaniza Aminudin,&nbsp;Noorlidah Abdullah","doi":"10.1016/j.prostaglandins.2025.107011","DOIUrl":"10.1016/j.prostaglandins.2025.107011","url":null,"abstract":"<div><div>Atherosclerosis is an inflammatory condition that contributes to myocardial infarction, cardiac arrest and stroke. Current knowledge of mushroom metabolomics in the context of atherosclerosis remains inadequate. Hence, further investigation into the underlying pathways and characterization of metabolites is necessary to establish a significant network for early-stage diagnosis of atherosclerosis. Therefore, the standard phytopreparation of <em>Schizophyllum commune</em> (SPPSC) was administered in hypercholesterolemic-induced rats. Sera were evaluated for lipid profile parameters; hepatic marker enzymes and the metabolic profile characterization was determined via liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (LC-QTOF-MS). SPPSC suppressed the elevation of cholesterol, LDL, triglyceride and atherogenic coefficient levels while increased HDL concentration and restored the function of hepatic antioxidant enzymes. The predictive accuracies and partial least square discriminant analysis (PLS-DA) revealed clear separation in metabolic features between normal, untreated, olive oil and SPPSC treated groups. Pathway analysis of the most significant metabolites targeted towards anti-atherosclerotic and cardio-protective activities were tryptophan metabolism, sphingolipid metabolism, β-alanine metabolism, taurine and hypotaurine metabolism, glutathione metabolism, phenylalanine metabolism, primary bile acid biosynthesis, histidine metabolism, pantothenate and CoA biosynthesis and cysteine and methionine metabolism. Identified metabolites indicate that <em>S. commune</em> is novel in preventing atherosclerosis and enhancing endogenous antioxidant system, protecting the cardiovascular system, minimalizing inflammation and regulating endothelial dysfunction.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"179 ","pages":"Article 107011"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of walnut consumption on biomarkers of oxidative stress: A systematic review and meta-analysis of randomized controlled trials","authors":"Vali Musazadeh ,&nbsp;Mahsa Mahmoudinezhad ,&nbsp;Niloofar Hamidi ,&nbsp;Maryam Falahatzadeh ,&nbsp;Farzad Shidfar","doi":"10.1016/j.prostaglandins.2025.106986","DOIUrl":"10.1016/j.prostaglandins.2025.106986","url":null,"abstract":"<div><div>Oxidative stress is caused by an imbalance between accumulation and production of oxygen reactive species (ROS) in tissues and cells and play a key role in many diseases. This systematic review and meta-analysis of randomized controlled trials (RCTs) was performed to analyze the effects of walnut consumption on biomarkers of oxidative stress. Databases including PubMed, Scopus, Embase and Web of science were searched until November 30th, 2024. Data were subjected to meta-analysis using a random effects model to examine the effect sizes of the pooled results. Four studies were identified eligible to be included in current meta-analysis. Walnut consumption resulted in a significant increase in catalase activity (CAT) (WMD: 42.20; 95 % CI: 34.28, 50.11). Walnut consumption did not affect other biomarkers of oxidative stress such as lipid peroxidation (LPO), reduced glutathione (GSH), oxidized glutathione (GSSG) and oxygen radical absorbance capacity (ORAC). Overall, this meta-analysis demonstrated walnut consumption increase CAT, but did not affect other biomarkers of oxidative stress. This suggests that walnut may have played an indirect and mild role in health. However, due to the limited number of studies, further investigations is suggested in this regard.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106986"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F7 upregulates MCM4 and fatty acid metabolism to advance lung adenocarcinoma metastasis","authors":"WuAsen Tang ,&nbsp;Deming Zhang ,&nbsp;Di Liu,&nbsp;Zikang Liu,&nbsp;Kuang Xiao,&nbsp;Chenggang Lei,&nbsp;Yalun Yang,&nbsp;Qian Zhou,&nbsp;Xianghui Wang","doi":"10.1016/j.prostaglandins.2025.106988","DOIUrl":"10.1016/j.prostaglandins.2025.106988","url":null,"abstract":"<div><h3>Background</h3><div>MCM4, a key protein in MCM, is frequently overexpressed in cancers, but its specific role in lung adenocarcinoma (LUAD) metastasis is unclear.</div></div><div><h3>Methods</h3><div>Bioinformatics revealed the mRNA expression pattern of MCM4 in LUAD, which we confirmed in both normal lung epithelial and adenocarcinoma cell lines using qRT-PCR and western blot (WB). Cellular proliferation was gauged by cell counting kit-8 and colony formation assays, and the expression of epithelial-mesenchymal transition markers along with fatty acid synthase (FASN) was probed via WB. We employed Transwell to assess cellular migration and invasion, and utilized kits for quantifying intracellular triglycerides and phospholipids. Bioinformatics identified E2F7 as a potential transcriptional regulator of MCM4, prompting us to explore its relationship with MCM4, including predicted binding sites and E2F7 mRNA expression in LUAD. Chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to validate the regulatory effects of E2F7 on MCM4.</div></div><div><h3>Results</h3><div>MCM4 was found to be overexpressed in LUAD, and its knockdown inhibited cancer cell proliferation, migration, invasion, and metastasis, along with decreased FASN expression and declined levels of triglycerides and phospholipids within cells. Mechanistically, E2F7 transcriptionally activated MCM4, regulating fatty acid metabolism and promoting LUAD progression and metastasis.</div></div><div><h3>Conclusion</h3><div>Our study elucidates the mechanism by which E2F7 transcriptionally controls MCM4 to activate fatty acid metabolism, fueling LUAD metastasis. These discoveries emphasize the pivotal function of lipid metabolism in LUAD development and suggests new therapeutic targets for LUAD treatment.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106988"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phagocytosis is differentially regulated by LPS in M1- and M2-like macrophages via PGE2 formation and EP4 signaling","authors":"Rebecca Kirchhoff,&nbsp;Michel André Chromik,&nbsp;Nils Helge Schebb","doi":"10.1016/j.prostaglandins.2025.106998","DOIUrl":"10.1016/j.prostaglandins.2025.106998","url":null,"abstract":"<div><div>Phagocytosis is a key process in human innate immune response. Human macrophages are important phagocytes engulfing and neutralizing pathogens and cell debris. In addition, they modulate the inflammatory process by releasing cytokines and lipid mediators. However, the link between oxylipins and phagocytosis in different macrophage phenotypes remains poorly understood. In order to better understand the link between phagocytosis and the arachidonic acid (ARA) cascade, we established a phagocytosis assay in primary human ‘inflammatory’ M1- and ‘anti-inflammatory’ M2-like macrophages from peripheral blood mononuclear cells (PBMC), representing extremes of macrophage phenotypes. The branches of the ARA cascade were investigated by quantitative targeted proteomics and metabolomics. M1-like macrophages show a higher abundance of cyclooxygenase (COX)-2 and its products particularly after LPS stimulus compared to M2-like macrophages. LPS increased phagocytosis in M2-like, but not in M1-like macrophages. We demonstrate that the COX product prostaglandin E2 (PGE₂) modulates the differential effects of LPS on phagocytosis: Via the EP4 receptor PGE₂ signaling suppresses phagocytosis in primary human macrophages. Thus, blockage of COX, e.g. by non-steroidal anti-inflammatory drugs (NSAID), leads to an increase of phagocytosis also in ‘inflammatory’ M1-like macrophages. This supports the well-described anti-inflammatory effects of these drugs and underscores the importance of the link between the COX branch of the ARA cascade and the regulation of phagocytosis in human macrophages.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106998"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased plasma lipoxin A4, resolvin D1, protectin D1 are correlated with the complexity and prognosis of coronary heart disease: A retrospective cohort study","authors":"Yun-fei Wang ,&nbsp;Xue-tao Zhu ,&nbsp;Ze-ping Hu","doi":"10.1016/j.prostaglandins.2025.106990","DOIUrl":"10.1016/j.prostaglandins.2025.106990","url":null,"abstract":"<div><div>This study aimed to assess the predictive capacity of specialized pro-resolving mediators (SPMs) regarding the complexity and prognosis of coronary heart disease (CHD). Total of 602 CHD patients were included in this study and categorized into low-risk, medium-risk, and high-risk groups based on the Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score. Follow-up was conducted for two years, during which patients were dichotomized into poor and good prognosis groups. Additionally, twenty healthy controls were incorporated. Plasma concentrations of lipoxin A4 (LXA4), resolvin D1 (RvD1), protectin D1 (PD1), C-reactive protein (CRP), interleukin-6 (IL-6), and IL-10 were quantified. Plasma LXA4, RvD1, PD1, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 exhibited a gradual decrease across control, low-risk, medium-risk, and high-risk groups and exhibited a negative correlation with the SYNTAX score. Spearman’s correlation analysis revealed negative correlations between plasma LXA4, RvD1, PD1, and both CRP and IL-6, and positive correlations with IL-10. Multiple linear regression models demonstrated negative associations between plasma LXA4, RvD1, PD1, and SYNTAX score. Moreover, both univariate and multivariate binary logistic regression analyses identified plasma LXA4, RvD1, and PD1 as protective factors against medium/high-risk SYNTAX score categorization. In the poor prognosis group, plasma PD1 was reduced at short-term follow-up, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were reduced at long-term follow-up. Plasma LXA4, RvD1, and PD1 demonstrated negative correlations with CHD complexity and potentially served as protective factors against CHD. Plasma PD1 provided predictive value for short-term prognosis, while the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were indicative for long-term prognosis.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106990"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of highly bioavailable forms of curcumin on lipoprotein(a) plasma levels: A systematic review and meta-analysis of randomized clinical studies","authors":"Federica Fogacci ,&nbsp;Ashot Avagimyan ,&nbsp;Arturo Cesaro ,&nbsp;Marco Bernardi ,&nbsp;Francesco Perone ,&nbsp;Marina Giovannini ,&nbsp;Arrigo Francesco Giuseppe Cicero","doi":"10.1016/j.prostaglandins.2025.106994","DOIUrl":"10.1016/j.prostaglandins.2025.106994","url":null,"abstract":"<div><div>Curcumin is a bioactive compound derived from the rhizome of <em>Curcuma longa</em> (turmeric) that has garnered increasing attention for its potential health benefits. However, its use in clinical practice is limited due to its generally poor bioavailability. This issue can be overcome using novel delivery systems that enhance curcumin’s solubility, extend its residence time in plasma, improve its pharmacokinetic profile, and increase its cellular uptake. Novel curcumin formulations with improved bioavailability have been suggested to elevate plasma concentrations of lipoprotein(a) (Lp(a)), but there is no definitive evidence of a causal relationship. To address this, a systematic literature search was conducted in multiple electronic databases to identify relevant randomized placebo-controlled clinical studies published without a time limit. A meta-analysis of data suggested that dietary supplementation with highly bioavailable forms of curcumin significantly reduces Lp(a) levels [Standardized Mean Difference (SMD)= -0.96 (95 % Confidence Interval (CI): −1.82, −0.11)]. The effect size was robust in the leave-one-out sensitivity analysis and was not primarily driven by any single study. Of course, the clinical significance of this observation should be more thoroughly evaluated in longer-term trials, where the combined metabolic and anti-inflammatory effects of curcumin have vascular protective effects.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106994"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143848655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protection of lutein against the toxic effect of cisplatin on liver in male rat","authors":"Ibrahim Aktas ,&nbsp;Fatih Mehmet Gur ,&nbsp;Sedat BILGIÇ","doi":"10.1016/j.prostaglandins.2025.106995","DOIUrl":"10.1016/j.prostaglandins.2025.106995","url":null,"abstract":"<div><h3>Objective</h3><div>A major challenge in cancer treatment is the detrimental effects of anticancer drugs on healthy organs and tissues. This study aims to investigate the protective effects of Lutein (LU) against Cisplatin (CT)-induced toxicity in rat liver, utilizing biochemical and histopathological assessments.</div></div><div><h3>Methods</h3><div>In this study, CT was administered intraperitoneally (i.p.) at a dose of 10 mg/kg, while LU was administered orally at a dose of 100 mg/kg. The experiment was conducted over a 7-day period with 28 male Sprague-Dawley rats (weighing 210–265 g, aged 11 weeks), divided into four groups (n = 7): Control, LU, CT, and CT + LU.</div></div><div><h3>Results</h3><div>CT-induced liver injury was identified as a dose-limiting side effect of CT. Compared to the CT group, the CT + LU group exhibited a significant decrease in malondialdehyde (MDA) levels and an increase in superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels. In the CT group, a significant increase in the levels of gamma-glutamyl transferase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) was observed, compared to the control group (p &lt; 0.05). When comparing the CT + LU group with the CT group, a significant reduction in the levels of GGT, ALT, AST, and LDH was observed (p &lt; 0.05). Histopathological analysis revealed liver damage in the CT group, characterized by leukocyte infiltration, sinusoidal dilatation, Councilman body formation, and hepatocellular degeneration and steatosis. In contrast, the CT + LU group exhibited only mild sinusoidal dilatation, with no other significant lesions. Immunohistochemical analysis showed positive staining for tumour necrosis factor-alpha (TNF-α) and caspase-3 in the liver tissue of CT group rats, which was significantly reduced in the CT + LU group. The staining pattern in the CT + LU group was similar to that of the control and LU groups.</div></div><div><h3>Conclusion</h3><div>The results of this study suggest that LU mitigates oxidative stress, enhances antioxidant defences, and supports liver function. Furthermore, LU demonstrates a protective effect against CT-induced liver damage, indicating its potential as a pharmacological agent for preventing CT-induced hepatic injury.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106995"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143874115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ceramide and DNA damage in liver fibrosis: Exploring the implications of eicosapentaenoic acid encapsulation in cellulose nanocrystals","authors":"Jihan Hussein ,&nbsp;Mona A. El-Bana ,&nbsp;Rehab A. Mohamed ,&nbsp;Enayat Omara ,&nbsp;Dalia Medhat","doi":"10.1016/j.prostaglandins.2025.106985","DOIUrl":"10.1016/j.prostaglandins.2025.106985","url":null,"abstract":"<div><div>Ceramide plays a crucial role in promoting liver fibrosis by inducing apoptosis and inflammation in hepatocytes. Oxidative stress accelerates fibrosis by elevating levels of urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), an indicator for the damage of DNA. We aimed to evaluate the efficacy of eicosapentaenoic acid encapsulated in cellulose nanocrystals (EPA-CNC) in inhibiting ceramide accumulation and reducing urinary 8-OHdG levels, thus providing protective effects against the progression of liver fibrosis.</div><div>In this study, twenty-four adult male Wistar albino rats were allocated into a negative control group, a group with liver fibrosis induced by diethylnitrosamine (DEN), and a group with DEN-induced liver fibrosis treated simultaneously with EPA-CNC. Key parameters assessed included liver paraoxonase-1 (PON-1), plasma interleukin-6 (IL-6), plasma ceramide, liver hydroxyproline (Hyp) content, and urinary 8-OHdG.</div><div>DEN-induced liver fibrosis led to a significant increase in inflammatory markers, including ceramide, IL-6, and notably urinary 8-OHdG. This was accompanied by a decrease in PON-1 activity and increased collagen deposition in liver tissues (Hyp content). Histopathological analysis revealed a substantial loss of liver architecture, with inflammation and fibrosis surrounding necrotic areas.</div><div>In contrast, treatment with encapsulated EPA-CNC resulted in a significant decrease in plasma ceramide, IL-6, liver Hyp content, and urinary 8-OHdG levels, along with an improvement in liver PON-1 activity. Histopathological findings showed nearly normal liver architecture.</div><div>In conclusion, increased levels of ceramide and urinary 8-OHdG could serve as indicators of ongoing hepatocellular damage due to their positive correlations with fibrotic markers. Encapsulated EPA-CNC may offer a promising approach for halting oxidative stress and inflammation in liver fibrosis.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106985"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances and challenges in lipid droplet isolation from animal tissues and cells","authors":"Yangli Pei,&nbsp;Siyu Wu,&nbsp;Zheng Feng","doi":"10.1016/j.prostaglandins.2025.106996","DOIUrl":"10.1016/j.prostaglandins.2025.106996","url":null,"abstract":"<div><div>Lipid droplets (LDs) are essential intracellular organelles involved in lipid storage and metabolism, playing critical roles in various cellular processes and diseases. Researchers require efficiently isolate and analyze LDs to understand lipid metabolism and related pathologies. This review summarizes recent advances in LD isolation methods, including traditional techniques such as centrifugation and density gradient centrifugation, as well as emerging technologies like automated and high-throughput approaches. We explore the applications of these methods in lipid metabolism research and discuss the challenges faced by current isolation techniques. Future directions, including automation, single-cell analysis, and integration with advanced analytical tools, are also highlighted to provide insights for the next generation of LD research.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106996"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}