Lipids in Health and Disease最新文献

{"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":"Elevated remnant cholesterol and triglycerides are predictors of increased total mortality in a primary health care population of 327,347 patients.","authors":"Anna Elise Engell, Lise Bathum, Volkert Siersma, Christen Lykkegaard Andersen, Bent Struer Lind, Henrik Løvendahl Jørgensen","doi":"10.1186/s12944-025-02607-5","DOIUrl":"10.1186/s12944-025-02607-5","url":null,"abstract":"<p><strong>Background: </strong>Hyperlipidemia is a well-established risk factor for cardiovascular disease and mortality. Recently, remnant cholesterol has been introduced as an important risk factor. This study explores the association between levels of remnant cholesterol, compared to the traditional lipid parameters (total cholesterol, low-density lipoprotein (LDL-C), high-density lipoprotein (HDL-C), non-high-density lipoprotein cholesterol (non-HDL-C) and triglycerides), and all-cause mortality in a population from general practice. Additionally, the impact of lipid-lowering treatment was evaluated.</p><p><strong>Methods: </strong>Observational cohort study based on the first lipid panel measurement from 327,347 patients from general practice in the Capital Region of Denmark between 2001 and 2018. LDL-C was calculated using the Friedewald equation. Patients with diagnoses or medical treatments that affected lipid levels were excluded. Cox proportional hazards models with restricted cubic splines were used to evaluate the association between all-cause mortality and lipid levels.</p><p><strong>Results: </strong>A total of 34,014 patients died during the study. In an analysis censoring individuals receiving lipid lowering treatment after the lipid measurement, remnant cholesterol increased all-cause mortality risk linearly, with a hazard ratio (HR) of 1.6 (95% CI: 1.4; 1.7) at 3 mmol/L compared to a reference level of 0.9 mmol/L. Total cholesterol showed a U-shaped relationship with all-cause mortality with a HR of 2.5 (95% CI: 2.3; 2.7) at 2.5 mmol/L and 1.7 (95% CI: 1.6; 1.9) at 9 mmol/L (reference level 5 mmol/L). LDL-C and non-HDL-C exhibited a very similar U-shaped pattern. HDL-C also showed a U-shaped curve with a HR of 1.7 (95% CI: 1.6; 1.9) at 0.5 mmol/L and 1.4 (95% CI: 1.3; 1.5) at 3.5 mmol/L (reference level 1 mmol/L). The mortality risk related to triglycerides increased with rising triglyceride level, with a HR of 1.5 (95% CI: 1.3; 1.6) at 4.5 mmol/L (reference level 2 mmol/L).</p><p><strong>Conclusions: </strong>In this study, high levels of all the six lipids as well as low levels of total cholesterol, LDL-C, non-HDL-C and HDL-C were associated with higher all-cause mortality in a primary health care population. Further research is needed, to consider if the current lipid lowering guidelines are appropriate and if more focus on remnant cholesterol levels should be applied.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"189"},"PeriodicalIF":3.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143161","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}

{"title":"Unlocking the lipid code: SREBPs as key drivers in gastrointestinal tumour metabolism.","authors":"Haowen Tang, Yuting Zhang, Danni Zhao, Minjie Guo, Xiao Yuan, Xu Wang","doi":"10.1186/s12944-025-02612-8","DOIUrl":"10.1186/s12944-025-02612-8","url":null,"abstract":"<p><p>In recent years, metabolic reprogramming has emerged as a significant breakthrough in elucidating the onset and progression of gastrointestinal (GI) malignancies. As central regulatory hubs for lipid metabolism, sterol regulatory element binding proteins (SREBPs) integrate dietary metabolic signals and carcinogenic stimuli through subtype-specific mechanisms, thereby promoting malignant tumour phenotypes. In this review, we first present the molecular background, structural characteristics, and posttranscriptional regulatory networks associated with SREBPs. We subsequently describe a systematic analysis of the distinct activation patterns of SREBPs in liver, gastric, colorectal, and other gastrointestinal cancers. Furthermore, we explore targeted intervention strategies for different SREBP subtypes, including small molecule inhibitors (such as fatostatin, which inhibits SREBP cleavage), natural compounds (such as berberine, which modulates the AMPK/mTOR pathway), and statin-mediated inhibition of the mevalonic acid pathway. These strategies may enhance tumour cell sensitivity to chemotherapeutic agents (such as 5-FU, gezil, and tabine) and improve the response to synergistic chemoradiotherapy by reversing adaptive metabolic resistance driven by the tumour microenvironment. Through this review, we hope to provide new insights into precise interventions targeting various subtypes of the SREBP molecule.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"190"},"PeriodicalIF":3.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143163","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 of serum uric acid-to-high-density lipoprotein cholesterol ratio with obstructive sleep apnea: a cross-sectional study.","authors":"Yan Tang, Jiaxin Liu, Junchi Zhang, Yuying Zhu, Jinling Zhou","doi":"10.1186/s12944-025-02604-8","DOIUrl":"10.1186/s12944-025-02604-8","url":null,"abstract":"<p><strong>Background: </strong>Characterized by intermittent hypoxia (IH), sleep fragmentation, and enhanced sympathetic nervous system activity, obstructive sleep apnea (OSA) precipitates oxidative stress, systemic inflammation, and metabolic perturbations. These disturbances manifest as alterations in serum uric acid (SUA) and high-density lipoprotein cholesterol (HDL-C) levels. Recently, the ratio of SUA to HDL-C (UHR) has emerged as a potential biomarker reflecting both inflammatory and metabolic status. This study investigates the association between UHR and OSA.</p><p><strong>Methods: </strong>Using a cross-sectional design, data were extracted from adults aged 20 years and older in the National Health and Nutrition Examination Survey (NHANES) database, covering the period from 2015 to March 2020. OSA was determined via the NHANES Sleep Disorders Questionnaire. The investigation employed weighted logistic regression alongside trend tests to evaluate the relationship between UHR and OSA. Nonlinear relationships were examined with restricted cubic spline analysis and threshold effect analysis. Receiver operating characteristic (ROC) curves were utilized to compare the predictive capacities of UHR, SUA, and HDL-C for OSA, with the area under the curve (AUC) calculated to assess the models' predictive accuracy. In addition, mediation analyses were conducted to explore the role of body mass index (BMI) in this association, and sensitivity analyses confirmed the robustness of the findings. Subgroup analyses further assessed the impact of various covariates.</p><p><strong>Results: </strong>Among the 9985 adults included, 4906 were identified as individuals with OSA. A positive association between UHR and the risk of OSA was observed (OR = 1.02; 95% CI: 1.01, 1.04; P = 0.014). Moreover, a nonlinear relationship was confirmed (P for nonlinearity = 0.024), with an inflection point at a UHR level of 10.23. UHR demonstrated greater predictive accuracy for OSA (AUC = 0.591) compared to SUA (AUC = 0.568) and HDL-C (AUC = 0.580). Additionally, BMI was found to partially mediate the relationship between UHR and OSA, with a mediation proportion of 61.99%. This association remained significant within specific subpopulations (P < 0.05) and was further modulated by factors such as age, alcohol consumption, and diabetes status (P for interaction < 0.05). Sensitivity analyses underscored the stability of these results.</p><p><strong>Conclusion: </strong>UHR is positively correlated with the risk of OSA in adults, with BMI serving as a partial mediator. The findings support UHR as a viable biomarker for early detection and risk assessment in patients with OSA. Strategies focusing on weight management may reduce the risk of OSA among individuals with elevated UHR levels.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"188"},"PeriodicalIF":3.9,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12102946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143159","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":"Long noncoding RNAs in familial hypercholesterolemia: biomarkers, therapeutics, and AI in precision medicine.","authors":"Hussam Daghistani, Gehan A Hegazy, Manal Alkhalofah, Afaf Alsobeihy, Sara Nasser, Hoda Gad, Taghreed Shamrani, Mohammed Mufrrih, Dareen Alyousfi","doi":"10.1186/s12944-025-02605-7","DOIUrl":"10.1186/s12944-025-02605-7","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have emerged as critical regulators of lipid metabolism, playing pivotal roles in cholesterol biosynthesis, transport, and efflux. Familial Hypercholesterolemia (FH), a genetic disorder characterized by excessive low-density lipoprotein cholesterol (LDL-C) levels, remains a significant contributor to premature cardiovascular disease (CVD). Traditional diagnostic methods, including lipid profiling and genetic testing, have limitations in sensitivity and accessibility, highlighting the need for novel molecular biomarkers. This review delves into the mechanistic involvement of lncRNAs in FH pathogenesis, shedding light on their potential as non-invasive biomarkers and therapeutic targets. Key lncRNAs such as LeXis, CHROME, and H19 have been implicated in cholesterol regulation and atherosclerosis progression, making them attractive candidates for precision medicine applications. Additionally, advancements in AI-driven lncRNA discovery and single-cell transcriptomics are paving the way for innovative diagnostic and therapeutic strategies. Emerging RNA-based therapeutics, including antisense oligonucleotides, small interfering RNAs (siRNAs), and CRISPR-based gene-editing tools, hold promise for modulating lncRNA function to restore lipid homeostasis. However, challenges such as biomarker validation, efficient RNA delivery, and regulatory approval must be addressed for clinical translation. The integration of lncRNA-based approaches into FH management offers new possibilities for early detection, targeted therapy, and personalized cardiovascular risk assessment, underscoring the need for continued research in this rapidly evolving field.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"182"},"PeriodicalIF":3.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119970","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":"Development and validation of a novel glucolipid metabolism-related nomogram to enhance the predictive performance for osteoporosis complications in prediabetic and diabetic patients.","authors":"Junhong Li, Cong Ma, Xinran Wang, Jianwen Li, Ping Liu, Meipeng Zhu","doi":"10.1186/s12944-025-02602-w","DOIUrl":"10.1186/s12944-025-02602-w","url":null,"abstract":"<p><strong>Background: </strong>Diabetes is the most prevalent metabolic disorder worldwide, imposing a significant economic burden on society. Prediabetes has not received as much attention as diabetes, and among its complications, osteoporosis has been relatively under-researched compared to cardiovascular disease. Recent studies have identified nine indices related to glucose and lipid metabolism that may enhance osteoporosis risk assessment in diabetic and prediabetic individuals. The research examined the osteoporosis risk prediction potential of these indices and developed a nomogram to enhance predictive performance.</p><p><strong>Methods: </strong>2,735 prediabetic and diabetic subjects were derived from National Health and Nutrition Examination Survey (NHANES) dataset collected between 2011 and 2020, then randomly assigned to development and validation cohorts in 7:3. The predictive capacity of glucolipid metabolism-related indices for osteoporosis risk was evaluated using receiver operating characteristic (ROC) curve analysis. The least absolute shrinkage and selection operator (LASSO) and multivariate logistic regression were used to identify predictors for constructing the risk model, which was visualized using a nomogram. The model's performance was further validated.</p><p><strong>Results: </strong>All the glucolipid metabolism-related indices showed predictive ability, and the best-performing index was metabolic score for insulin resistance (METS-IR). Multivariate logistic regression identified 5 predictors [Triglyceride-glucose index (TyG), age, METS-IR, TyG-waist circumference, and TyG-body mass index] with good predictive performance. These predictors were selected to establish the nomogram. ROC curve, calibration plot, as well as decision curve analysis (DCA) collectively demonstrated fairly good predictive ability of the nomogram.</p><p><strong>Conclusions: </strong>Glucolipid metabolism-related indices are the predictors of osteoporosis risk. This newly developed nomogram based on glucolipid metabolism indices demonstrates optimal predictive accuracy for assessing combined osteoporosis risk in individuals with prediabetes and diabetes.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"183"},"PeriodicalIF":3.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093595/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120226","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":"Emerging risks of lipid-lowering therapy and low LDL levels: implications for eye, brain, and new-onset diabetes.","authors":"Erkan Cure, Medine Cumhur Cure","doi":"10.1186/s12944-025-02606-6","DOIUrl":"10.1186/s12944-025-02606-6","url":null,"abstract":"<p><p>Atherosclerotic cardiovascular disease remains a major global health burden. Current guidelines emphasize aggressive lipid-lowering strategies, particularly those that reduce low-density lipoprotein cholesterol (LDL-C) levels. While effective in lowering cardiovascular risk, excessively low LDL-C may have unintended health consequences. LDL-C plays a critical physiological role in cellular structure and hormone synthesis. Emerging evidence links low LDL-C and high HDL-C with increased glaucoma risk. Statins, which are commonly used to lower LDL-C, may further increase this risk, raising concerns for patients with coronary artery disease. Low LDL-C has also been associated with gestational diabetes and intracranial hemorrhage, while statin therapy may contribute to new-onset diabetes mellitus. These findings highlight the need to reassess the \"lower is better\" paradigm. A patient-centered, risk-based approach to statin therapy is recommended. Large-scale randomized controlled trials are urgently needed to establish safe lipid thresholds and optimize therapeutic strategies.</p>","PeriodicalId":18073,"journal":{"name":"Lipids in Health and Disease","volume":"24 1","pages":"185"},"PeriodicalIF":3.9,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12093843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119442","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}