Current opinion in lipidology最新文献

Emerging regulators of endothelial lipid metabolism in atherosclerosis. 动脉粥样硬化中内皮脂质代谢的新调控因子。

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-02-09 DOI: 10.1097/MOL.0000000000001031

Jason S Irei, Kai Hirayama, William A Boisvert

{"title":"Emerging regulators of endothelial lipid metabolism in atherosclerosis.","authors":"Jason S Irei, Kai Hirayama, William A Boisvert","doi":"10.1097/MOL.0000000000001031","DOIUrl":"10.1097/MOL.0000000000001031","url":null,"abstract":"Purpose of review: Although therapies for hyperlipidemia and hypertension have been shown to be highly effective, they have not sufficiently mitigated overall cardiovascular disease risk. Endothelial cells (ECs) are an integral mediator in the development and progression of atherosclerotic cardiovascular disease. The purpose of this review is to provide an update on the current state of endothelial lipid metabolism research, with particular emphasis on atherosclerosis.Recent findings: Although it has been known that elevated palmitic acid (PA) levels were linked to metabolic dysfunction, inflammation and cardiovascular diseases, more recent studies presented here elucidate the mechanisms behind the negative effects induced by PA. Palmitoylation was found to be detrimental in the case of pyruvate kinase isozyme M2 (PKM2) activity, but also vital for the normal functioning of endothelial ciliation and cell health. Endothelial cholesterol metabolism and hemodynamic forces have also been further confirmed to be key regulators in vessel development and endothelial homeostasis. Perturbations in these pathways promote endothelial dysfunction and maladaptive lipid accumulation.Summary: Although atherosclerosis remains a complex, multifactorial disease that arises from the coordinated dysfunction across multiple vascular and immune cell types, substantial advances have been made in identifying mechanisms behind dysfunctional endothelial lipid metabolism. Despite this, further investigation is necessary to identify high impart therapeutic targets aimed at reducing overall cardiovascular disease risk.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"113-119"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polygenic risk scores in familial hypercholesterolemia. Do they have a role? 家族性高胆固醇血症的多基因风险评分。他们有角色吗？

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-02-13 DOI: 10.1097/MOL.0000000000001029

Martine Paquette, Simon-Pierre Guay, Alexis Baass

{"title":"Polygenic risk scores in familial hypercholesterolemia. Do they have a role?","authors":"Martine Paquette, Simon-Pierre Guay, Alexis Baass","doi":"10.1097/MOL.0000000000001029","DOIUrl":"10.1097/MOL.0000000000001029","url":null,"abstract":"Purpose of review: Risk assessment in patients with familial hypercholesterolemia (FH) remains an important clinical challenge. The polygenic susceptibility for plasma lipoprotein traits or coronary artery disease (CAD) can be assessed by polygenic risk scores (PRS). The purpose of this review is to discuss the potential roles of PRS in the context of FH management.Recent findings: Recent studies suggested that a high PRS for lipoprotein(a) falsely explains the phenotype in a fifth of variant-negative FH patients, whereas a larger proportion can be explained by high low-density lipoprotein cholesterol (LDL-C) PRS. The cardiovascular risk, but also the risk of type 2 diabetes, is different in patients with polygenic hypercholesterolemia compared to monogenic FH. Lastly, it has been shown that a PRS for CAD, but not for LDL-C or lipoprotein(a), was associated with increased lifelong incidence of cardiovascular disease in patients with monogenic FH, independently of clinical variables.Summary: Several studies have explored the potential clinical relevance of PRS in FH, including for diagnostic purpose and in cardiovascular risk stratification. Prior to implementation in clinical practice for cardiovascular risk stratification, future studies in FH should determine whether the polygenic information offers incremental predictive value over conventional clinical variables.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"107-112"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A JAK of two trades: beneficial or adverse effects of Janus kinase inhibition for plasma LDL-cholesterol and major adverse cardiovascular events in inflammatory bowel disease patients? 两个行业的JAK：抑制Janus激酶对炎症性肠病患者血浆ldl -胆固醇和主要不良心血管事件的有利或不利影响？

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-04-07 DOI: 10.1097/MOL.0000000000001040

Katherine Muñoz Ayala, Eleonora A M Festen, Marit Westerterp

{"title":"A JAK of two trades: beneficial or adverse effects of Janus kinase inhibition for plasma LDL-cholesterol and major adverse cardiovascular events in inflammatory bowel disease patients?","authors":"Katherine Muñoz Ayala, Eleonora A M Festen, Marit Westerterp","doi":"10.1097/MOL.0000000000001040","DOIUrl":"10.1097/MOL.0000000000001040","url":null,"abstract":"Purpose of review: Janus kinase (JAK) inhibitors have emerged as potent anti-inflammatory drugs and are prescribed in rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). However, cardiovascular safety concerns have emerged from RA safety trials, alongside increases in LDL cholesterol (LDL-c). Whether similar lipid changes in IBD translate into clinically meaningful cardiovascular risk remains uncertain. This review focuses on studies and mechanisms increasing LDL-c due to JAK inhibition in IBD.Recent findings: JAK inhibitors increase plasma LDL-c levels in IBD patients in a dose-dependent manner. While this has generally been attributed to JAK inhibitors decreasing inflammation, inhibition of JAK signaling also decreases hematopoiesis: the differentiation of hematopoietic stem cells into granulocyte/macrophage progenitors, and subsequently neutrophils, monocytes, and macrophages. Hematopoiesis requires LDL-c uptake, and is associated with elevated plasma LDL-c when inhibited. While statins lower LDL-c, the high prevalence of metabolic syndrome-associated type 2 diabetes in IBD patients may prompt the use of alternative lipid-lowering drugs.Summary: JAK inhibitors are associated with increased LDL-c levels in IBD patients which may be due to suppressed inflammation and decreased hematopoiesis. This review summarizes the evidence on lipid changes and cardiovascular outcomes upon JAK inhibition and discusses approaches for LDL-c management in IBD.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":"37 3","pages":"120-130"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lipoprotein(a) in familial hypercholesterolemia. 家族性高胆固醇血症的脂蛋白(a)

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-02-10 DOI: 10.1097/MOL.0000000000001032

Ali K Jaafar, Steeve Bourane, Gilles C Lambert, Kevin Chemello

{"title":"Lipoprotein(a) in familial hypercholesterolemia.","authors":"Ali K Jaafar, Steeve Bourane, Gilles C Lambert, Kevin Chemello","doi":"10.1097/MOL.0000000000001032","DOIUrl":"10.1097/MOL.0000000000001032","url":null,"abstract":"Purpose of review: Elevated concentrations of both low-density lipoprotein (LDL)-cholesterol and lipoprotein(a) [Lp(a)] is probably the most detrimental lipid profile in terms of cardiovascular health. Our primary objective was to review the reports published before January 2026 pertaining to the metabolism of lipoprotein(a) and associated cardiovascular disease (CVD) risk specifically in familial hypercholesterolemia.Recent findings: Lp(a) has consistently been found elevated in familial hypercholesterolemia (FH) cohorts. To a large extent, this results from the fact that elevated Lp(a) increases the likelihood for a patient to be clinically diagnosed as FH. For long, increases in Lp(a) concentrations observed in FH patients have been regarded as the consequence of impaired Lp(a) plasma clearance by the LDL receptor. However, recent studies strongly advocate against a significant role for the LDL receptor in mediating Lp(a) hepatic uptake. The molecular mechanisms by which Lp(a) is cleared from blood still remain elusive. Finally, mounting clinical evidence indicates that lowering LDL-C pharmacologically will not offset the specific cardiovascular risk stemming from elevated Lp(a) in FH.Summary: It is highly recommended to systematically measure Lp(a) in FH patients. These patients should be treated with high-dose statins, when necessary, in combination with a proprotein convertase subtilisin/kexin type 9 inhibitor to reach LDL-C therapeutic goals. Hopefully, the Lp(a) lowering therapies currently under development will prove instrumental for adequate treatment of FH patients with concomitantly elevated Lp(a) in coming years.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"93-99"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNA interference for lipid disorders: is this the future? RNA干扰治疗脂质紊乱：这是未来吗？

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-02-09 DOI: 10.1097/MOL.0000000000001033

Miguel Nassif, Renata Turrini Jacob Fazoli, Giuliano Generoso

{"title":"RNA interference for lipid disorders: is this the future?","authors":"Miguel Nassif, Renata Turrini Jacob Fazoli, Giuliano Generoso","doi":"10.1097/MOL.0000000000001033","DOIUrl":"10.1097/MOL.0000000000001033","url":null,"abstract":"Purpose of review: Advances in the management of lipid disorders have expanded therapeutic options for hypercholesterolemia and beyond. We review the current advances in RNA interference (RNAi) therapies as small interfering RNA (siRNA) drugs, critically assess their clinical positioning, and explore their potential role in reshaping lipid management over the next years.Recent findings: RNAi enables targeted, durable suppression of key lipid-regulating proteins at the mRNA level. Inclisiran, the first approved RNAi therapy for hypercholesterolemia, achieves about 50% sustained LDL-c reduction with long-interval maintenance dosing, offering an alternative to monoclonal antibodies. Beyond LDL-c lowering, multiple RNAi drugs are in advanced development targeting lipoprotein(a), apolipoprotein C-III, and angiopoietin-like protein 3, aiming to address residual cardiovascular risk. Early safety and adherence data are encouraging, yet pivotal outcome trials and cost-effectiveness analyses are still pending.Summary: RNAi is a naturally occurring gene-silencing mechanism that can be harnessed therapeutically through siRNA molecules. In lipidology, siRNA-based therapies represent a disruptive technology with the potential to transform both prevention and treatment of atherosclerotic cardiovascular disease. If ongoing trials confirm cardiovascular benefit and safety, RNAi agents could become foundational in personalized lipid management, moving the field toward long-acting, target-specific, and potentially combination-based regimens. The coming years will determine whether RNAi fulfills its promise as the future standard of care in lipid disorders.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"86-92"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inflammation and atherosclerotic cardiovascular disease: where do we go from here? 炎症和动脉粥样硬化性心血管疾病：我们将何去何从？

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-04-14 DOI: 10.1097/MOL.0000000000001039

Ori Waksman, Ron Waksman

{"title":"Inflammation and atherosclerotic cardiovascular disease: where do we go from here?","authors":"Ori Waksman, Ron Waksman","doi":"10.1097/MOL.0000000000001039","DOIUrl":"10.1097/MOL.0000000000001039","url":null,"abstract":"Purpose of review: Low-grade systemic inflammation, as determined by high-sensitivity C-reactive protein (hsCRP), plays a significant role in the progression and development of atherosclerotic cardiovascular disease (ASCVD) and is recognized as a risk enhancer for increased incidence of major adverse cardiovascular events (MACE). In 2024, the US Food and Drug Administration approved colchicine, as the first anti-inflammatory agent for secondary cardiovascular prevention. While this step signified a translational milestone, recent neutral colchicine trials, such as CLEAR- SYNERGY, have reignited controversy regarding the overall efficacy of colchicine, and the need for alternative anti-inflammatory therapies. As the understanding of inflammation's role in atherosclerosis grows, questions persist about the best management strategies and future therapeutic options. This review aims to provide an updated summary that includes insights from recent key trials, explores investigational anti-inflammatory treatments, and discusses considerations for future trial designs.Recent findings: This review will encompass recent trials involving colchicine, IL-1 antagonists, and interluekin-6 inhibitors.Summary: In this review, we will discuss mechanisms of inflammation as they pertain to ASCVD, significant contemporary trials, novel anti-inflammatory therapies, and considerations for future trial designs.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"79-85"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HDL and ASCVD: is high HDL-C protective, harmful, or simply misleading? HDL和ASCVD：高HDL- c是保护、有害还是误导？

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-06-01 Epub Date: 2026-04-07 DOI: 10.1097/MOL.0000000000001041

Paolo Parini, Matteo Pedrelli

{"title":"HDL and ASCVD: is high HDL-C protective, harmful, or simply misleading?","authors":"Paolo Parini, Matteo Pedrelli","doi":"10.1097/MOL.0000000000001041","DOIUrl":"10.1097/MOL.0000000000001041","url":null,"abstract":"Purpose of review: This review examines whether high high-density lipoprotein cholesterol (HDL-C) is protective, harmful, or simply misleading in relation to atherosclerotic cardiovascular disease (ASCVD), with emphasis on recent mechanistic, epidemiologic, genetic, and trial evidence.Recent findings: HDL is biologically important and multifunctional, but HDL-C is an imperfect surrogate for HDL function. Recent cohort studies show nonlinear associations, with very high HDL-C not consistently protective and in some settings associated with increased mortality. Mendelian randomization studies do not support HDL-C as a causal protective factor, and randomized trials of HDL-C-raising strategies have generally failed to reduce ASCVD events. These findings have shifted attention from HDL quantity to HDL quality, including cholesterol efflux capacity, particle characteristics, and pathway-specific biology. At the same time, modern cholesteryl ester transfer protein (CETP) inhibition has renewed interest in whether benefit, if any, relates to Apolipoprotein B-lowering rather than HDL-C elevation itself.Summary: HDL biology remains highly relevant, but HDL-C alone should not be interpreted as a reliable marker of atheroprotection or as a therapeutic target. Very high HDL-C should not be used to downplay established causal risk factors. Future research should prioritize functional HDL metrics, deeper phenotyping, and mechanism-aligned trials to determine whether improving HDL quality, rather than simply raising HDL-C, can reduce ASCVD risk.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"100-106"},"PeriodicalIF":4.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147632837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Update on genetics of familial hypercholesterolemia. 家族性高胆固醇血症的遗传学研究进展。

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-04-01 Epub Date: 2026-02-10 DOI: 10.1097/MOL.0000000000001027

Tomas Freiberger

{"title":"Update on genetics of familial hypercholesterolemia.","authors":"Tomas Freiberger","doi":"10.1097/MOL.0000000000001027","DOIUrl":"10.1097/MOL.0000000000001027","url":null,"abstract":"Purpose of review: Familial hypercholesterolemia is a monogenic Mendelian disorder characterized by elevated LDL cholesterol and premature atherosclerotic cardiovascular disease. It is caused by pathogenic variants in LDLR , APOB , and PCSK9 , with rarer involvement of LDLRAP1 and APOE . Despite advances in molecular diagnostics, no causative variant is identified in approximately 25-75% of clinically diagnosed cases.Recent findings: Familial hypercholesterolemia is currently defined as an autosomal semi-dominant disorder with a gene-dosage effect, whereby biallelic pathogenic variants result in markedly more severe phenotypes than heterozygous variants. Terminology for homozygous familial hypercholesterolemia has been refined. Former terms such as 'true homozygote', 'compound heterozygote', and 'double heterozygotes' have been replaced by monogenic biallelic forms, with identical or different variants, and digenic biallelic forms involving two familial hypercholesterolemia-associated genes. Polygenic risk score (PRS) and lipoprotein(a) measurement help explain familial hypercholesterolemia-like phenotypes in patients without a monogenic cause and enable determination of polygenic severe hypercholesterolemia and/or hyperlipoproteinemia(a). Although advances in molecular genetics have improved variant detection, interpretation remains challenging. Integration of case-level data and functional studies, including high-throughput LDLR assays and APOB structural analyses, has enhanced variant pathogenicity classification.Summary: Combining monogenic variant detection, PRS determination and lipoprotein(a) assessment enables comprehensive diagnosis, tailored risk stratification, and personalized familial hypercholesterolemia management.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"38-44"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Recent advances in understanding the spectrum of genetic determinants of lipoprotein(a) levels. 脂蛋白(a)水平遗传决定因素谱的最新研究进展。

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-04-01 Epub Date: 2026-02-06 DOI: 10.1097/MOL.0000000000001030

Stefan Coassin

{"title":"Recent advances in understanding the spectrum of genetic determinants of lipoprotein(a) levels.","authors":"Stefan Coassin","doi":"10.1097/MOL.0000000000001030","DOIUrl":"10.1097/MOL.0000000000001030","url":null,"abstract":"Purpose of review: Our understanding of the genetic regulation of lipoprotein(a) [Lp(a)] is hindered by the complex structure of the LPA gene, limited non-European datasets and its elusive cellular receptor(s). This review summarizes recent efforts and advances providing new insights on its genetic architecture, variability across ancestries and regulators beyond the LPA gene.Recent findings: Impressive advances in DNA sequencing and bioinformatics now resolve LPA variants and kringle IV-type 2 copy number at scale. This provides new reference datasets and enables tools that unlock hidden variation also from already available sequencing datasets. In parallel, genetic studies broaden our understanding of the regulation of Lp(a) across ancestries and improve genetic risk scores. Finally, while recent studies implicate new mechanisms for Lp(a) uptake, upcoming genome-wide gene knockout screens allow comprehensive, agnostic scans for regulators and receptors. Puzzlingly, this still converges on the LDL receptor, whose exact role in Lp(a) uptake remains enigmatic.Summary: Technological advances establish a foundation for more accurate genetic risk assessment across ancestries. These advances are enhancing our understanding of Lp(a) regulation and build a framework for future integrative genetic studies, which may shed new light on the evolution of the Lp(a) trait, adding important context for its physiological and clinical relevance.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"65-72"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146141285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic determinants of plasma lipids in Greenlanders. 格陵兰人血脂的遗传决定因素。

IF 4.6 3区医学

Current opinion in lipidology Pub Date : 2026-04-01 Epub Date: 2026-01-09 DOI: 10.1097/MOL.0000000000001023

Jasmin Hjerresen, Emil Jørsboe, Mette K Andersen

{"title":"Genetic determinants of plasma lipids in Greenlanders.","authors":"Jasmin Hjerresen, Emil Jørsboe, Mette K Andersen","doi":"10.1097/MOL.0000000000001023","DOIUrl":"10.1097/MOL.0000000000001023","url":null,"abstract":"Purpose of review: Greenlanders differ from other populations in terms of traditional lifestyle and genetic architecture. This might have a great impact on lipid levels in the population and the spectrum of genetic variants associated with lipid traits. Here, we review recent advances in lipid genetics in Greenlanders and highlight the potential of moving from single lipid trait analyses to more comprehensive lipidomic profiling.Recent findings: Genetic association studies in the Greenlandic population have identified variants, including PCSK9 (rs12117661), LDLR (rs730882082), and SI (rs781470490), associated with large effects on triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, and total cholesterol (TC) levels, as well as altered risk of cardiovascular disease (CVD). These variants are common in the Greenlandic population and explain more lipid variation than variants observed in Europeans. Accordingly, European-derived polygenic scores (PGSs) underperform in Greenlanders, but including the Greenlandic variants increases the performance of lipid PGSs. Lipidomic profiling has the potential to reveal strong cardiometabolic-risk signatures.Summary: The Greenlandic population harbors high-impact variants in PCSK9 , LDLR , and SI, particularly affecting the levels of TG, LDL-C, and TC. Obtaining information on these variants could facilitate earlier detection and potentially prevention of CVD, and advance precision medicine for Greenlanders.","PeriodicalId":11109,"journal":{"name":"Current opinion in lipidology","volume":" ","pages":"30-37"},"PeriodicalIF":4.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0