Lipids in Health and Disease最新文献

{"title":"High fat diet exacerbated glycolipid metabolism disorder in kidney Yang deficiency rats by interfering with IRS 1-PI3K (p85) -Akt-GLUT 4 pathway.","authors":"Han Li, Yunqiao Wang, Wei Zheng, Jing Lu, Cuiyao Tang, Mengyang Long, Bo Liu, Bin Chen, Weihong Li, Zihui Xu","doi":"10.1186/s12944-025-02721-4","DOIUrl":"https://doi.org/10.1186/s12944-025-02721-4","url":null,"abstract":"<p><strong>Background: </strong>Kidney Yang deficiency (KYD) is associated with disturbances in glucose and lipid metabolism. This study examined whether KYD rats on a high-fat diet (HFD) exhibit aggravated metabolic dysfunction and sought to elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>Three-week-old SD rats were assigned to control (Con), KYD, HFD, and KYD + HFD groups. KYD models were induced through cold exposure and gastric perfusion of Cortex Phellodendri. The HFD groups were provided high-fat diets. After 10 weeks, metabolic parameters, organ weights, blood glucose/lipid profiles, and protein levels (PGC1α, PPARγ, IRS1, Akt, PI3K(p85), GLUT4) were assessed.</p><p><strong>Results: </strong>KYD rats exhibited lower body temperature, weight, and weight gain (P< 0.01) compared to controls. Liver weight was reduced in the KYD group but increased in the HFD group (P< 0.01). KYD + HFD rats demonstrated increased visceral fat (P < 0.01) and decreased muscle mass. The KYD + HFD group showed a higher liver-to-body weight ratio (P < 0.05) and significantly elevated cholesterol and LDL levels (P< 0.01 vs. other groups). Muscle PPARγ was lower in the KYD group, while the AUC of glucose tolerance was elevated in the KYD + HFD group (P< 0.05). GLUT4 and PI3K(p85) levels were reduced in both KYD and HFD groups (P < 0.01，P<0.01). IRS1 expression in skeletal muscle was lower in both KYD and HFD groups (P < 0.01) but was higher in KYD compared to HFD (P < 0.01). Akt expression was marginally increased in KYD and significantly higher in HFD groups.</p><p><strong>Conclusions: </strong>KYD predisposes rats to visceral fat accumulation, dyslipidemia, and fatty liver despite lower weight gain. Mechanistically, the impairment of the IRS1-Akt-PI3K(p85)-GLUT4 signaling pathway in KYD compromises insulin action, exacerbating lipid metabolic disturbances under HFD. These findings highlight the dietary risks for individuals with KYD and emphasize the need for targeted interventions aimed at specific metabolic pathways.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"313"},"PeriodicalIF":3.9,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145251764","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":"Chronic hypoxia induces liver injury via PKCδ/ASMase-driven ceramide accumulation and endoplasmic reticulum stress in rats.","authors":"Yujie Huang, Yu Ding, Xiaoyu Guo, Lingfang Huang, Xiangqiong Meng, Wenjun Jiang, Zejun Wang, Tian Yang, Minghai Zheng, Xiaoling Tan","doi":"10.1186/s12944-025-02761-w","DOIUrl":"10.1186/s12944-025-02761-w","url":null,"abstract":"","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"312"},"PeriodicalIF":3.9,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244680","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":"Lipid accumulation product and visceral adiposity index in polycystic ovary syndrome: a systematic review and meta-analysis of observational studies.","authors":"Mohammadamin Parsaei, Elaheh Karimi, Amirali Barkhordarioon, Mohammadreza Yousefi, Azadeh Tarafdari","doi":"10.1186/s12944-025-02719-y","DOIUrl":"10.1186/s12944-025-02719-y","url":null,"abstract":"<p><strong>Background: </strong>Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder associated with reproductive and metabolic dysfunction. Emerging evidence indicates that the lipid accumulation product (LAP) and visceral adiposity index (VAI) could be valuable indicators for evaluating metabolic dysfunction. This study aims to compare LAP and VAI between women with PCOS and healthy controls to evaluate their potential role in metabolic risk assessment.</p><p><strong>Methods: </strong>A structured database search was carried out on March 18, 2025, using PubMed, Web of Science, Scopus, and Embase. Observational studies comparing LAP/VAI levels between women with PCOS and healthy controls were included. Risk of bias was assessed using the Joanna Briggs Institute checklists. A random-effects meta-analysis was carried out to evaluate the pooled differences in LAP and VAI levels between individuals with PCOS and those in the control group. Subgroup analyses were conducted based on the PCOS phenotypes (A, B, C, and D) defined by the Rotterdam criteria and the body mass index categories (lean and overweight/obese).</p><p><strong>Results: </strong>Fifty studies (13,741 women) were analyzed, with 41 included in the meta-analysis. LAP (32 studies: Cohen's d = 0.597 [0.469-0.726]; P-value < 0.001; I² = 88.22%) and VAI (28 studies: Cohen's d = 0.457 [0.378-0.537]; P-value < 0.001; I² = 65.16%) were significantly higher in PCOS women, with calculated pooled values of 37.1 vs. 23.9 and 3.1 vs. 2.6, respectively. Subgroup analyses revealed that LAP lost significance across all phenotypes (P-value > 0.05), while VAI remained elevated in phenotypes A (P-value < 0.001), B (P-value = 0.001), and D (P-value = 0.001), with marginal significance in C (P-value = 0.051). Stratified by body mass index, LAP was non-significant in lean women (P-value = 0.083) but higher in overweight/obese women (P-value = 0.001). Conversely, VAI was significantly elevated in both lean and overweight/obese groups (P-value = 0.001 each).</p><p><strong>Conclusions: </strong>This study demonstrates significantly higher levels of LAP and VAI in patients with PCOS compared to controls. These readily calculable indices may serve as practical tools for metabolic risk stratification in PCOS populations. However, further research is needed to establish their diagnostic accuracy and validate their clinical utility.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"311"},"PeriodicalIF":3.9,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12506430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244715","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":"Breaking the metabolic-inflammatory vicious cycle in polycystic ovary syndrome: a comparative review of ketogenic and high-fat diets.","authors":"Wenwen Yang, Nan Pang, Xiaoxia He","doi":"10.1186/s12944-025-02693-5","DOIUrl":"10.1186/s12944-025-02693-5","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is a multifactorial metabolic-endocrine disorder in women of reproductive age in which lipid metabolism disorders and chronic low-grade inflammation reinforce and amplify each other. Recently, the ketogenic diet (KD), which is a high-fat, very-low-carbohydrate dietary intervention, has drawn attention because of its metabolic regulation and anti-inflammatory properties. This review integrates current evidence to elucidate how aberrant fatty acid turnover, adipose tissue dysfunction, and adipokine imbalance trigger convergent proinflammatory pathways, thus forming an \"inflammatory hub\" that links insulin resistance, hyperandrogenemia, impaired folliculogenesis, and heightened cardiovascular risk in PCOS. The mechanisms by which strict carbohydrate restriction promotes fatty acid β-oxidation and hepatic ketogenesis are delineated, thereby reprogramming cellular metabolism. The principal ketone body, β-hydroxybutyrate, directly suppresses the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 inflammasome, remodels the gut microbiota, and attenuates nuclear factor kappa-light-chain-enhancer of activated B cells signaling, thus yielding multitarget anti-inflammatory effects. Unlike isocaloric high-fat diets, which lead to obesity, inflammation, and insulin resistance, the KD lowers triacylglycerols and the proportion of small, dense low-density lipoprotein particles; enhances whole-body insulin sensitivity; and mitigates systemic inflammation. Collectively, the KD offers a multidimensional intervention that couples metabolic correction with immune modulation and holds promise for improving PCOS trajectories and long-term complications. Nevertheless, its long-term safety profile, lipid subclass optimization, and biomarker-driven personalization require further investigation.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"310"},"PeriodicalIF":3.9,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238984","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":"The joint effect of triglyceride-glucose index and C-reactive protein levels on the risk of chronic obstructive pulmonary disease: a prospective cohort study.","authors":"Jialiu He, Mengxia Li, Pengfei Luo, Zheng Zhu, Jian Su, Ran Tao, Jinyi Zhou, Ming Wu, Xikang Fan","doi":"10.1186/s12944-025-02732-1","DOIUrl":"10.1186/s12944-025-02732-1","url":null,"abstract":"<p><strong>Background: </strong>The triglyceride-glucose index (TyG) and C-reactive protein (CRP) are key biomarkers on clinical diagnosis, each related to lung dysfunction. However, the relationship of both indexes with the risk of chronic obstructive pulmonary disease (COPD) is still unclear. This study purposes to focus on the individual and joint associations of TyG and CRP levels with COPD risk.</p><p><strong>Methods: </strong>This cohort study utilized baseline TyG and CRP data from the UK Biobank. Hazard ratios (HRs) and 95% confidence intervals (CIs) for COPD risk associated with TyG and CRP levels were calculated through Cox regression models. Receiver operating characteristic (ROC) curves were conducted to determine the optimal cut-off values for TyG and CRP, which were combined into a joint variable. Kaplan-Meier (KM) method was utilized to analyze cumulative hazard, while joint analysis was employed for evaluating the joint risk. Stratified and sensitivity analyses were also performed to assess the associations within subgroups, and mediation effect of TyG on COPD risk via CRP levels was assessed.</p><p><strong>Results: </strong>This study enrolled 385,523 individuals, with 10,515 COPD cases were recorded in follow-up. Compared to the lowest quintile, individuals with higher TyG and CRP had increased risk of COPD (all HRs > 1.00). The optimal cut-off values of TyG and CRP were 7.14 and 1.88 mg/L, and we found that the simultaneous elevation of both TyG and CRP significantly increased the risk of COPD. Moreover, the joint effect was stronger in participants younger than 60 years old, males, smokers or passive smokers, those with body mass index (BMI) < 25.0 kg/m², and those without baseline diabetes, asthma, or a family history of respiratory diseases (P _{for interaction} < 0.05). Moreover, the effect of TyG on COPD was significantly mediated by CRP, explaining almost 15.6% of this influence.</p><p><strong>Conclusions: </strong>These results underscored the individual and joint effects of TyG and CRP upon COPD risk, indicating their usefulness as biomarkers for early risk assessment.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"309"},"PeriodicalIF":3.9,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238933","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":"Visceral fat area loss reduces 10-year atherosclerotic cardiovascular disease risk in Chinese population with type 2 diabetes mellitus: a prospective cohort study.","authors":"Jing Jin, Yu Lei, Jia Zheng, Jinjian Xu, Linna Chen, Shuning Liu, Xingyue Cao, Ye Hu, Chenyan Yan, Xiaohong Wu","doi":"10.1186/s12944-025-02711-6","DOIUrl":"10.1186/s12944-025-02711-6","url":null,"abstract":"<p><strong>Background: </strong>Among individuals diagnosed with type 2 diabetes mellitus (T2DM), an abnormal accumulation of visceral fat heightens the cardiovascular risk (CVR), and the major reason for death for these people is atherosclerotic cardiovascular disease (ASCVD). This study aimed to gain further insights into the longitudinal relationship between CVR and visceral fat area (VFA) in patients with T2DM, and to compare the predictive performance of additional abdominal obesity measures and VFA for changes in CVR.</p><p><strong>Methods: </strong>This prospective cohort study included 316 patients with T2DM who were followed up for more than one year, and VFA was measured by the bioimpedance method. This study investigated the prospective association between a VFA percentage change (∆VFA, %) and CVR, and evaluated the potential nonlinear relationships between ∆VFA (%) and the increase 10-year ASCVD risk. Furthermore, the area under the pooled curve (AUC) was contrasted for both ∆VFA (%) and other abdominal obesity indices.</p><p><strong>Results: </strong>The excessive VFA loss group showed lower low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol (TC), triglyceride-glucose index, LDL-C/HDL-C, brachial-ankle pulse wave velocity, 10-year ASCVD risk, atherogenic index of plasma, TC/HDL-C, and apolipoproteins B/apolipoproteins A-1 than the VFA gain group (all β [Formula: see text] 0, HR [Formula: see text] 1, all P [Formula: see text] 0.05) after covariate controlling. VFA reduction of more than 14.82% led to a reduction in the stated risk. Moreover, ∆VFA (%) demonstrated superior predictive value for changes in ASCVD risk, with an AUC of 0.585 (95% CI: 0.513-0.656), compared to other obesity indices.</p><p><strong>Conclusions: </strong>Excessive VFA reduction improved 10-year ASCVD risk in patients diagnosed with T2DM. VFA was a more effective predictor of 10-year ASCVD risk changes than other abdominal obesity measures.</p><p><strong>Trial registration: </strong>This investigation has been registered with the Chinese Clinical Trial Registry (ChiCTR2400086569).</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"308"},"PeriodicalIF":3.9,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12498462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238945","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":"MLN4924 inhibits macrophage foam cell formation by enhancing autophagy and regulating metabolic phenotype.","authors":"Lei Xing, Yu Bu, Jingqi Shi, Jing Liu, Fan Hu, Minghua Zhang, Jiao Fan","doi":"10.1186/s12944-025-02683-7","DOIUrl":"10.1186/s12944-025-02683-7","url":null,"abstract":"","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"307"},"PeriodicalIF":3.9,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12492866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213161","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":"Excessive cholesterol accelerates intervertebral disc degeneration by promoting the polarization of M1 macrophages.","authors":"Sheng-Jie Chang, Hao-Wei Xu, Shu-Bao Zhang, Xiao-Wei Liu, Yu-Yang Yi, Shan-Jin Wang","doi":"10.1186/s12944-025-02709-0","DOIUrl":"10.1186/s12944-025-02709-0","url":null,"abstract":"<p><strong>Background: </strong>Intervertebral disc degeneration (IVDD) is the primary cause of low back pain (LBP). Dyslipidaemia can induce a chronic inflammatory state in the body, promote the polarization of macrophages, and may affect the homeostasis of the intervertebral disc (IVD). However, the relationship between dyslipidaemia and IVDD remains unclear.</p><p><strong>Methods: </strong>This study encompassed human subjects and animal models. Techniques used: cell counting kit-8 (CCK8), western blotting, immunofluorescence staining, immunohistochemical staining, flow cytometry, enzyme-linked immunosorbent assay (ELISA), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and statistical analysis.</p><p><strong>Results: </strong>Through a retrospective analysis involving 196 patients, this study found that high TC, TG, and LDL-C levels were risk factors for IVDD. Subsequently, cell experiments and animal models verified that excessive cholesterol can directly induce the loss of phenotype in nucleus pulposus cells and promote the M1-type polarization of macrophages through the JAK1/STAT1 pathway, thereby accelerating IVDD.</p><p><strong>Conclusions: </strong>These results reveal that excessive cholesterol is a risk factor for intervertebral disc degeneration, emphasizing its direct role in the degeneration process as well as its involvement in signal regulation during macrophage polarization. Therefore, cholesterol-lowering therapy may provide new opportunities for the treatment of IVDD.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"305"},"PeriodicalIF":3.9,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12490159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145206755","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":"Association between volatile organic compounds in urine and dyslipidemia: findings based on analysis of NHANES data.","authors":"Lili Wu, Zhihang Ma, Yan Ma, Jing Gao","doi":"10.1186/s12944-025-02731-2","DOIUrl":"10.1186/s12944-025-02731-2","url":null,"abstract":"<p><strong>Background: </strong>Evidence linking urinary metabolites of volatile organic compounds (UMVOCs) to dyslipidemia remains limited and scarce. This research sought to thoroughly clarify the UMVOCs-dyslipidemia associations and evaluate the inflammation's mediating effect in this association.</p><p><strong>Methods: </strong>Nationally representative data (from 6,962 enrolled participants) obtained from the National Health and Nutrition Examination Survey (NHANES) formed the basis of this analysis. We applied weighted logistic regression models for the assessment of relationship between individual UMVOC exposure and dyslipidemia, and weighted quantile sum (WQS) regression for the evaluation of the impact of co-exposure to multiple mixed UMVOCs on dyslipidemia. We performed mediation analysis for investigation into inflammation's role as a mediator, with white blood cell count (WBC), neutrophil count (NC), as well as lymphocyte count (LC) incorporated for the evaluation of their respective contributions to the overall mediation effect.</p><p><strong>Results: </strong>Urinary concentrations of 34MHA and CEMA were positively linked to dyslipidemia, with respective odds ratios (OR) of 1.10 (95% confidence interval [CI]: 1.00-1.21) and 1.21 (95% CI: 1.08-1.35). Furthermore, through WQS regression analysis, we found that exposure to a mixture of 16 UMVOCs was significantly and positively linked to dyslipidemia (OR = 1.14, 95% CI: 1.04-1.24, P = 0.002), with CEMA making the greatest relative contribution (29.75%). Mediation analysis demonstrated that WBC, NC, and LC partially mediated the association between CEMA and dyslipidemia, accounting for 10.35%, 6.54%, and 6.52% of the total mediation effects, respectively (all P < 0.001).</p><p><strong>Conclusion: </strong>Simultaneous exposure to multiple UMVOCs is positively and significantly linked to the prevalence of dyslipidemia, with inflammation partially mediating this relationship. Our findings suggest that prolonged or high-level exposure to UMVOCs may contribute to dyslipidemia through inflammatory pathways, underscoring the potential metabolic health risks posed by environmental pollutants.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"306"},"PeriodicalIF":3.9,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12492794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213115","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":"Cotrimoxazole use is associated with lower total and non-high density lipoprotein cholesterol among people with HIV: a cross-sectional study.","authors":"Joseph Baruch Baluku, Martin Nabwana, Ronald Olum, George Patrick Akabwai, Felix Bongomin","doi":"10.1186/s12944-025-02722-3","DOIUrl":"10.1186/s12944-025-02722-3","url":null,"abstract":"","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"304"},"PeriodicalIF":3.9,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12487471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145199802","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}