Lipids in Health and Disease最新文献

{"title":"Correlation between Castelli risk index-I and female infertility: A cross-sectional study.","authors":"WeiJing Yang, XingLong Liu, YuChan Wang, YaLu Fu, ChunE Ren, AiFang Jiang, YuHan Meng","doi":"10.1186/s12944-025-02617-3","DOIUrl":"10.1186/s12944-025-02617-3","url":null,"abstract":"<p><strong>Background: </strong>The association between metabolic syndrome and female reproductive health has garnered increasing attention; however, the relationship between the Castelli risk index I (CRI-I, total cholesterol/high-density lipoprotein cholesterol ratio) and infertility remains unclear. This study was designed to explore the potential association between CRI-I and female infertility.</p><p><strong>Methods: </strong>The study population was derived from data collected in three consecutive two-year cycles (2013-2018) of the National Health and Nutrition Examination Survey (NHANES), ultimately including 2,629 female participants aged 18-45 years. Weighted multivariable logistic regression models were used to assess the association between CRI-I and infertility following adjustment for covariates such as demographic characteristics, medical history, and lifestyle factors, among others. Restricted cubic spline and threshold effect analyses were conducted to examine possible nonlinear associations. Subgroup analyses and ROC curves were used to assess robustness and predictive capacity.</p><p><strong>Results: </strong>CRI-I scores were significantly elevated in the infertile group in comparison with the non-infertile group (median [interquartile range, IQR]: 3.38 [2.77-4.07] vs. 3.08 [2.53-3.80]; P = 0.001). CRI-I showed a positive monotonic association with infertility risk, with each unit increase corresponding to a 17% higher likelihood (adjusted OR = 1.17, 95% CI: 1.01-1.36; P = 0.042). Nonlinear analysis identified a threshold effect between CRI-I and infertility risk (inflection point = 3.73): the risk increased significantly when CRI-I was < 3.73 (OR = 1.54, 95% CI: 1.20-1.98), whereas the association attenuated above this threshold. Subgroup analysis revealed a significant interaction by hypertension status (interaction P < 0.05). CRI-I demonstrated modest predictive utility for female infertility (AUC = 0.580, 95% CI: 0.548-0.613).</p><p><strong>Conclusions: </strong>Elevated CRI-I scores were positively associated with female infertility, particularly in specific subgroups (e.g., younger, married, non-hypertensive, or alcohol-consuming individuals). These findings underscore the potential role of dysregulated lipid metabolism in female reproductive dysfunction.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"200"},"PeriodicalIF":3.9,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12131381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216254","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":"Targeting intramyocellular lipids to improve aging muscle function.","authors":"David W Russ, Ravikumar Manickam, Srinivas M Tipparaju","doi":"10.1186/s12944-025-02622-6","DOIUrl":"10.1186/s12944-025-02622-6","url":null,"abstract":"<p><p>Decline of skeletal muscle function in old age is a significant contributor to reduced quality of life, risk of injury, comorbidity and disability and even mortality. While this loss of muscle function has traditionally been attributed to sarcopenia (loss of muscle mass), it is now generally appreciated that factors other than mass play a significant role in age-related muscle weakness. One such factor gaining increased attention is the ectopic accumulation of lipids in skeletal muscle, in particular, intramyocellular lipids (IMCLs). It has been appreciated for some time that metabolic flexibility of several tissues/organs declines with age and may be related to accumulation of IMCLs in a \"vicious cycle\" whereby blunted metabolic flexibility promotes accumulation of IMCLs, which leases to lipotoxicity, which can then further impair metabolic flexibility. The standard interventions for addressing lipid accumulation and muscle weakness remain diet (caloric restriction) and exercise. However, long-term compliance with both interventions in older adults is low, and in the case of caloric restriction, may be inappropriate for many older adults. Accordingly, it is important, from a public health standpoint, to pursue potential pharmacological strategies for improving muscle function. Because of the success of incretin-analog drugs in addressing obesity, these medications may potentially reduce IMCLs in aging muscles and thus improve metabolic flexibility and improve muscle health. A contrasting potential pharmacological strategy for addressing these issues might be to enhance energy provision to stimulate metabolism by increasing NAD + availability, which is known to decline with age and has been linked to reduced metabolic flexibility. In this narrative review, we present information related to IMCL accumulation and metabolic flexibility in old age and how the two major lifestyle interventions, caloric restriction and exercise, can affect these factors. Finally, we discuss the potential benefits and risks of select pharmacologic interventions in older adults.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"197"},"PeriodicalIF":3.9,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191957","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 ratio of blood urea nitrogen to high-density lipoprotein cholesterol: a novel risk-stratifying tool for infective endocarditis.","authors":"Qi Wang, Jing-Wen Li, Shuai-Zheng Che, Jie-Leng Huang, Mei Jiang, Jun-Quan Lu, Di Wu, Dan-Qing Yu, Xue-Biao Wei","doi":"10.1186/s12944-025-02595-6","DOIUrl":"10.1186/s12944-025-02595-6","url":null,"abstract":"<p><strong>Background: </strong>Increased blood urea nitrogen (BUN) and decreased high-density lipoprotein cholesterol (HDL) are common in infectious diseases. However, the prognostic significance of the BUN-to-HDL ratio (BHR) in patients with infective endocarditis (IE) is yet unknown.</p><p><strong>Methods: </strong>In all, 1441 patients with confirmed IE were included and divided into four groups according to the level of BUN and HDL: BUN > 5.2mmol/L and HDL < 0.7mmol/L (n = 296), BUN > 5.2mmol/L and HDL ≥ 0.7mmol/L (n = 364), BUN ≤ 5.2mmol/L and HDL < 0.7mmol/L (n = 327), and BUN ≤ 5.2mmol/L and HDL ≥ 0.7mmol/L (n = 454). BHR was calculated as BUN/HDL. Multivariable analyses were conducted to determine the association of BHR with adverse events.</p><p><strong>Results: </strong>The in-hospital mortality was 6.4%. Patients with BUN > 5.2mmol/L and HDL < 0.7mmol/L had a significantly higher risk of in-hospital death than those with BUN ≤ 5.2mmol/L and HDL ≥ 0.7mmol/L (adjusted odds ratio [aOR] = 4.65, 95% confidence interval [CI]: 1.91-11.35, p = 0.001). The decision curve analysis indicated that the combination of BUN and HDL had higher net benefit than either alone. BHR presented a higher predictive value than BUN (AUC: 0.744 vs 0.693, p = 0.01) or HDL (AUC: 0.744 vs 0.648, p < 0.001) for in-hospital mortality, and the optimal cut-off value was 7.4 (sensitivity, 79.3%; specificity, 60.3%). Furthermore, the cumulative 6-month mortality risk was significantly higher in patients with BHR > 7.4 than those with BHR ≤ 7.4 (log-rank = 93.4, p < 0.001). BHR > 7.4 was an independent risk factor for 6-month mortality in IE (adjusted hazard ratio [aHR] = 3.77, 95%CI: 2.32-6.11, p < 0.001).</p><p><strong>Conclusions: </strong>BHR offers a high predictive value for short-term mortality in IE, positioning it as a potential stratification tool for critical care triage.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"196"},"PeriodicalIF":3.9,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187318","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":"Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver.","authors":"Lijuan Chen, Guoyuan Sui, Jin Wu, Ning Li, Zhe Zhang, Ying Du, Meijun Lü, Xiaorui Yan, Guowei Pan, Lianqun Jia","doi":"10.1186/s12944-025-02613-7","DOIUrl":"10.1186/s12944-025-02613-7","url":null,"abstract":"<p><strong>Background: </strong>Micro/nanoplastics (MNPs), as emerging environmental pollutants, are widely present in environments that are essential for human survival. They exist in vast quantities and possess stable properties, making them challenging to manage. Some reports indicated that there is a positive correlation between the production of MNPs and the incidence of obesity. The liver serves as both the central hub for lipid metabolism and a prime target for MNPs toxicity. These studies revealed that MNPs can lead to increased hepatic lipid accumulation, suggesting that they may be potential obesogens. However, the specific metabolic changes and possible mechanisms involved remain to be elucidated.</p><p><strong>Methods: </strong>This study focuses on the impact of nanoplastics (NPs) on liver lipid metabolism, using C57BL/6J mice (hereinafter referred to as C57 mice) as the research subjects, and exposing them to 100 nm NPs at 1000 µg/L continuously for 12 weeks.</p><p><strong>Results: </strong>The study revealed that (1) NPs led to nondietary weight gain together with an increase in fat volume and mass in mice. (2) NPs significantly increased serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels, with notable differences between groups. Notably, NPs exposure induced opposing effects on serum lipid profiles, elevating high-density lipoprotein cholesterol (HDL-C) concentrations while suppressing triglyceride (TG) levels, though intergroup differences failed to reach statistical significance. (3) NPs caused multiple inflammatory responses in the liver, with significant lipid deposition. (4) Untargeted metabolomics analysis indicated that NPs exposure led to significant alterations in various lipid metabolites, particularly glycerophospholipids. Additionally, transcriptomics reveals that differentially expressed genes (DEGs) triggered by NPs exposure are predominantly involved in metabolic routes including lipid metabolism and cytochrome P450 (CYP). Taken together, these findings suggested that alterations in lipid metabolism resulting from NPs exposure may involve arachidonic acid metabolism. Phosphatidylcholine (PC) could be the key substance, and the CYP gene family (Cyp2c23, Cyp2c40) might be the critical genes regulating liver lipid metabolism during NPs exposure.</p><p><strong>Conclusions: </strong>This study has demonstrated that NPs exposure induced obesity and hepatic lipid accumulation in male mice independently of food intake. The integrated omics data identified dysregulated PC metabolism and CYP gene family expression, suggesting their involvement in arachidonic acid-associated pathways. These findings provided preliminary mechanistic clues linking NP exposure to hepatic lipid metabolism dysregulation and helped to elucidate the adverse effects of NPs on liver lipid metabolism.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"195"},"PeriodicalIF":3.9,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181864","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":"Inflammation mediates the relationship between cardiometabolic index and vulnerable plaque in patients with acute coronary syndrome.","authors":"Haihao Yan, Sai Lv, Haiyao Pi, Haixu Yu, Weijun Yin, Yaran Wang, Yonghao Lan, Wei Liu","doi":"10.1186/s12944-025-02608-4","DOIUrl":"10.1186/s12944-025-02608-4","url":null,"abstract":"<p><strong>Background: </strong>As a novel indicator reflecting metabolic status and visceral adiposity distribution, the cardiometabolic index (CMI) has gained attention in cardiovascular risk stratification. This investigation employed optical coherence tomography (OCT) to examine potential associations between CMI and vulnerable plaque, as well as the role of inflammation.</p><p><strong>Methods: </strong>This study conducted a cross-sectional analysis of 270 acute coronary syndrome (ACS) patients who had OCT imaging evaluation. Patients were categorized based on CMI tertiles, with CMI calculated using the formula [waist (cm)/height (cm)]×[triglycerides (mmol/L)/HDL-C (mmol/L)]. OCT was used to assess plaque events in culprit lesions and plaque components in non-culprit lesions, and inflammatory markers were measured. A mediation analysis framework was implemented to investigate inflammatory pathways in CMI-vulnerable plaque relationships.</p><p><strong>Results: </strong>CMI tertiles were linked to vulnerable plaque traits: thin-cap fibroatheromas (TCFA), macrophages (Tertiles1 vs. Tertiles2 vs. Tertiles3, TCFA: 10.0% vs. 20.0% vs. 26.7%, P = 0.016; macrophages: 17.8% vs. 28.9% vs. 36.7%, P = 0.019). Multivariate regression demonstrated CMI elevation independently predicted a higher prevalence of TCFA (OR:1.40, 95%CI: 1.25-2.89, P = 0.003), more macrophage infiltration (OR:1.61, 95% CI:1.09-2.37, P = 0.017), reduced FCT (β:-30.65, 95% CI:-50.72-10.57, P = 0.003), and enlarged maximum lipid arc (β:20.78, 95% CI:6.55-35.01, P = 0.004). Moreover, CMI was positively related to hsCRP, WBC, and neutrophils. Mediation analysis revealed that hsCRP mediated about 17.0% of the association between CMI and minimum FCT [Indirect effect=-5.21, 95% CI=(-12.70, -1.27), P = 0.016].</p><p><strong>Conclusions: </strong>CMI is a key forecaster of vulnerable plaque in patients with ACS. Systemic inflammation is associated with the relationship between CMI and vulnerable plaque features, suggesting a potential mechanistic link.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"194"},"PeriodicalIF":3.9,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174348","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 mediating effect of maternal blood lipids on the association between maternal exposure to PM_2.5 and birth weight: a retrospective birth cohort study in Zhejiang, China.","authors":"Huiqi Chen, Qinqing Chen, Danxiao Wang, Min Lv, Liyun Wang, Yuan Chen, Fangfang Xi, Hefeng Huang, Qiong Luo","doi":"10.1186/s12944-025-02614-6","DOIUrl":"10.1186/s12944-025-02614-6","url":null,"abstract":"<p><strong>Background: </strong>Maternal PM_2.5 exposure and lipid levels during pregnancy were independently detected associated with birth weight. Potential mediating factors still remain unclear.</p><p><strong>Methods: </strong>This study aimed to examine the association of maternal PM_2.5 exposure and birth weight, and explore the potential mediation effect of maternal blood lipids in the relationship between PM_2.5 exposure and birth weight. 5,162 pregnant women from Zhejiang, China were included in the study during 2013-2014. We measured blood lipids for each participant in the second and third trimesters. Air pollution exposure in residential districts was estimated based on satellite data for each individual throughout three trimesters in pregnancy. Linear mixed-effects models were employed to examine associations between PM_2.5 and birth weight. Using a mediation analysis approach, we decomposed the total effect of PM_2.5 on birth weight into natural direct and indirect effects via blood lipid concentration.</p><p><strong>Results: </strong>After adjusting for covariates, a 10 µg/m³ increment in PM_2.5 during the second trimester was directly associated with an 11.65 g increase in birth weight (95% CI: 2.99, 20.31 g). The indirect effects of PM_2.5 exposure (each 10 µg/m³ increase) on birth weight, mediated through elevated maternal lipid levels, were - 2.35 g (95% CI: -4.07, -0.63 g) for total cholesterol to high-density lipoprotein cholesterol ratio (TC: HDL ratio), -0.69 g (95% CI: -1.16, -0.22 g) for Triglycerides (TG), and - 1.80 g (95% CI: -3.19, -0.41 g) for HDL-C, during the second trimester.</p><p><strong>Conclusions: </strong>Findings suggest prenatal PM_2.5 exposure may impact term birth weight via direct biological effects and lipid-mediated pathways, underscoring the importance of incorporating air pollution mitigation into perinatal care and advancing biomarker-driven fetal monitoring. Future research should clarify PM_2.5 component-specific effects, decode placental-fetal lipid regulatory mechanisms, and validate pollution-metabolism-outcome relationships through multi-regional cohorts to inform precision environmental health interventions and clinical risk management.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"193"},"PeriodicalIF":3.9,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144159830","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":"Lipoprotein (a) levels and clinical decision-making: data from a Mexican cohort at a tertiary medical institution.","authors":"Ivette Cruz-Bautista, Yuscely Flores-Jurado, Guillermo Roa-Álvarez, Mariana Salas-Aldana, Daniel Benjamin Elías-Lopez, Ricardo Federico Hernández-Franco, Sandra Rosales-Uvera, Arsenio Vargas-Vázquez, Raymundo Valdez-Echeverría, Sonia Luna Del Villar Velasco, Liliana Muñoz-Hernández, Roopa Mehta, Mario Morales-Esponda, Misael Aguilar-Panduro, Guillermo Chan-Puga, Adrián Soto Mota, Carlos Alberto Aguilar-Salinas","doi":"10.1186/s12944-025-02610-w","DOIUrl":"10.1186/s12944-025-02610-w","url":null,"abstract":"<p><strong>Background and objective: </strong>Approximately 20% of the global population has a Lp(a) concentrations above 50 mg/dL (> 125nmol/L), yet many remain unaware of the associated cardiovascular risks. In Mexico, routine measurement of Lp(a) is uncommon. This study aimed to investigate the frequency of Lp(a) testing, and the clinical actions taken by physicians upon detecting elevated Lp(a) concentrations in patients at a tertiary medical institution.</p><p><strong>Methods: </strong>Using an algorithm-based screening system, we reviewed the clinical and biochemical data of patients with Lp(a) measurements from 2019 to 2024. Data were retrieved from the laboratory information system and electronic health records. Complementary assessment data were obtained from the radiology and cardiology departments.</p><p><strong>Results: </strong>Of the 150,083 individuals evaluated at the institution, only 830 (0.5%) underwent Lp(a) testing, with testing rates increasing from 0.037% in 2019 to 0.24% in 2023. Elevated Lp(a) concentrations (> 50 mg/dL) were found in 21% of patients, and 2.2% had concentrations > 180 mg/dL. Patients with elevated Lp(a) had significantly higher rates of atherosclerotic cardiovascular disease (ASCVD) (p < 0.001) and familial hypercholesterolemia (p < 0.004) than those with lower Lp(a) levels. Interestingly, diabetes prevalence was higher in those with Lp(a) < 4 mg/dL (51.5% vs. 33.4%, p < 0.001). Despite the cardiovascular risk, only 26% of patients with elevated Lp(a) levels received interventions to modify risk factors.</p><p><strong>Conclusions: </strong>Lp(a) testing was infrequent in a tertiary medical setting. Clinical interventions to modify cardiovascular risk factors were insufficient among patients with elevated Lp(a). These findings highlight the need for greater awareness among healthcare providers and the development of comprehensive screening and management algorithms to mitigate Lp(a) -related cardiovascular risk.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"192"},"PeriodicalIF":3.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150988","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 association between the uric acid-to-high-density lipoprotein cholesterol ratio and osteoarthritis risk in U.S. adults: a cross-sectional study based on NHANES 1999-2016.","authors":"Yaoxin Ao, Fangjun Xiao, Junpeng Qiu, Jiangfeng Lyu, Wenli Luo, Yifei Liufu, Junxing Yang","doi":"10.1186/s12944-025-02618-2","DOIUrl":"10.1186/s12944-025-02618-2","url":null,"abstract":"<p><strong>Objective: </strong>The uric acid-to-high-density lipoprotein cholesterol ratio (UHR) is an established biomarker for metabolic and inflammatory disorders but has received little attention in relation to osteoarthritis (OA). This investigation examines the UHR‒OA risk correlates.</p><p><strong>Methods: </strong>This cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) 1999-2016. Descriptive analyses, univariate and multivariate logistic regression models, as well as generalized additive and segmented regression models were used to investigate the nonlinear correlation and threshold effect of UHR-OA.</p><p><strong>Results: </strong>A total of 20,727 U.S. adults were included, 2,900 of whom (13.99%) were diagnosed with osteoarthritis (OA). A nonlinear relationship with a significant threshold effect was observed between the UHR and OA. When the UHR was less than 0.109, it was strongly inversely related to OA (OR = 0.028, 95% CI: 0.002-0.345, P < 0.01). The odds ratio increased when the UHR surpassed 0.109 but was not statistically significant (OR = 0.625, 95% CI: 0.162-2.421, P > 0.05). According to the unadjusted logistic regression model, the UHR was not significantly correlated with OA (P > 0.05). Following adjustment for confounders, including sex, age, ethnicity, education, marriage, BMI, income, hypertension, diabetes, coronary heart disease, and hypercholesterolemia, a notable inverse relationship emerged (OR = 0.259, 95% CI: 0.093-0.718, P < 0.01). Univariate linear regression studies revealed an intense inverse relationship between UA and HDL-C (OR = -3.2, 95% CI: -3.3 to -3.0, P < 0.001). In addition, stratified studies revealed that the negative relationships between the UHR and OA were more pronounced in elderly individuals (≥ 50 years old), women, drinkers, non-Hispanic whites, individuals with higher education levels and individuals without metabolic disorders (those with no hypertension, diabetes, coronary heart disease, or hypercholesterolemia) and did not show obvious heterogeneity in smoking status, BMI, marriage, or income level.</p><p><strong>Conclusions: </strong>This study revealed a nonlinear relationship between the UHR and OA, with a threshold at UHR = 0.109. Below this level, the UHR was significantly negatively associated with OA, especially in older adults (≥ 50 years old), females, drinkers, non-Hispanic Whites, and those with an education level above high school, or no metabolic diseases.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"191"},"PeriodicalIF":3.9,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150990","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":"Dehydrodiisoeugenol alleviates palmitate-induced mitochondrial dysfunction in human vascular smooth muscle cells through the activation of SIRT1-mediated Drp1 deacetylation.","authors":"Jianjun Zhao, Zhiyun Shu, Xiangjun Li, Wenqing Zhang, Mengze Sun, Wenxiao Song, Hongyuan Cheng, Shaomin Shi","doi":"10.1186/s12944-025-02611-9","DOIUrl":"10.1186/s12944-025-02611-9","url":null,"abstract":"<p><strong>Objective: </strong>Dehydrodiisoeugenol (Deh) has demonstrated positive effects in the prevention and treatment of cardiovascular disease (CVD) caused by lipid overload, but its specific mechanism of action remains poorly understood. The aim of this study was to investigate the possible mechanisms by which Deh modulates the mitochondrial dysfunction induced by palmitate (PA) in vascular smooth muscle cells (VSMCs).</p><p><strong>Methods: </strong>A PA-induced high-fat model of VSMCs was established, and the effect of PA on the VSMCs on function was detected by evaluating the oxidative stress and apoptosis of cells, as well as mitochondrial function. The expression of dynamin-related protein 1 (Drp1) was detected by immunofluorescence and immunoprecipitation. The key targets of Deh for the treatment of mitochondria-related diseases were screened by bioinformatics analysis and molecular docking techniques. Finally, the role of Silent information regulator 1 (SIRT1) in the treatment of PA-induced mitochondrial dysfunction in VSMCs by Deh was explored by administrating Deh as well as SIRT1 activator (CAY10602, CAY) and SIRT1 inhibitor (JGB1741, JGB).</p><p><strong>Results: </strong>The results showed that PA concentration-dependently increased oxidative stress and apoptosis in VSMCs, while modulating the acetylation of Drp1, promoting its expression and mitochondrial ectopia, thereby inducing mitochondrial dysfunction. Bioinformatics analysis and molecular docking indicated that SIRT1 may be a key target of Deh for the treatment of mitochondria-related diseases. Follow-up experiments revealed that Deh significantly inhibited PA-induced mitochondrial dysfunction in VSMCs by suppressing acetylation and expression of Drp1 and reducing mitochondrial ectasia, an effect that was achieved by regulating SIRT1.</p><p><strong>Conclusion: </strong>Deh was able to inhibit Drp1 expression and mitochondrial ectopia by reducing Drp1 acetylation through activation of SIRT1, thereby inhibiting PA-induced mitochondrial dysfunction effects in VSMCs, ameliorating pathological processes, such as cellular oxidative stress and apoptosis, and maintaining stable cellular functions.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"187"},"PeriodicalIF":3.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143160","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":"Lipoprotein(a) and panvascular disease.","authors":"Ruiyan Xu, Zhenwei Wang, Jiayu Dong, Miao Yu, Yue Zhou","doi":"10.1186/s12944-025-02600-y","DOIUrl":"10.1186/s12944-025-02600-y","url":null,"abstract":"<p><p>Panvascular disease (PVD) is an emerging clinical concept that encompasses a spectrum of atherosclerotic conditions involving multiple major vascular beds, including the coronary, cerebral, peripheral, and valvular arteries. Although not formally recognized as a nosological entity, in this review, PVD is adopted as a conceptual framework to reflect the systemic nature of atherosclerosis affecting vascular territories supplying the heart, brain, and peripheral circulation. This perspective enables a more integrated understanding of disease processes across organ systems that are often studied in isolation. Lipoprotein(a) [Lp(a)] is a genetically regulated, low-density lipoprotein (LDL)-like particle that has garnered increasing attention as an independent pathogenic risk factor for PVD. Accumulating evidence from epidemiological, genetic, and mechanistic studies has confirmed the multifaceted role of Lp(a) in promoting atherogenesis, vascular calcification, inflammation, and thrombogenesis across multiple vascular beds. Elevated Lp(a) levels are associated with increased cardiovascular and cerebrovascular event risk, even after controlling for traditional risk factors. This review systematically outlines the structure, genetic determinants, and pathogenic mechanisms of Lp(a), and synthesizes current clinical evidence regarding its role in various PVD subtypes. The interactions between Lp(a) and traditional cardiovascular risk factors such as hypercholesterolemia, diabetes, and hypertension are explored in depth, highlighting their synergistic contributions to vascular injury and disease progression. Furthermore, sex-based differences in Lp(a)-associated risk, response to therapy, and biological behavior are discussed, providing insights into personalized cardiovascular risk stratification. In addition, the review summarizes current and emerging therapeutic strategies targeting Lp(a), including niacin, antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), and gene-editing technologies. These advances offer promising new avenues for reducing residual cardiovascular risk attributable to elevated Lp(a). In conclusion, viewing Lp(a)-associated pathology through the lens of PVD provides a comprehensive and unifying approach to understanding its systemic impact. This framework supports the development of integrated risk assessment tools and multi-targeted interventions, ultimately aiming to improve outcomes for patients with complex, multisite vascular involvement.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"186"},"PeriodicalIF":3.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143162","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}