{"title":"Discrepant Effect of High-Density Lipoprotein Cholesterol on the Hematologic Malignancy Risk: A Nationwide Cohort Study.","authors":"Su Youn Nam, Junwoo Jo, Won Kee Lee","doi":"10.12997/jla.2025.14.1.94","DOIUrl":"10.12997/jla.2025.14.1.94","url":null,"abstract":"<p><strong>Objective: </strong>Although high-density lipoprotein cholesterol (HDL-C) is inversely associated with hematologic malignancies, modification by smoking has not been reported. We investigated how smoking and menopausal status modify these association.</p><p><strong>Methods: </strong>This population-based cohort study enrolled cancer-free individuals who underwent a national cancer screening in 2010 and followed up until December 2017. HDL-C levels were classified into eight groups based on 10 mg/dL intervals: (<30, 30-39, 40-49, 50-59, 60-69, 70-79, 80-89, or ≥90 mg/dL).</p><p><strong>Results: </strong>Among 4,517,892 participants, 5887 had lymphoma, 3348 had leukemia, and 12151 had unspecified hematologic malignancies. The adjusted hazard ratios (aHRs) for the lowest HDL-C levels compared to the 70-79 mg/dL range were 1.83 (1.45-2.31) for lymphoma, 3.14 (2.41-4.08) for leukemia, and 2.34 (2.01-2.72) for unspecified hematologic malignancy. The effects of low HDL-C levels on hematologic malignancies were similar in both men and women. Low HDL-C levels were associated with a higher risk of leukemia regardless of smoking status, but extremely high HDL-C levels were linked to a higher risk of leukemia (aHR, 2.32; 95% confidence interval [95% CI], 1.18-4.55) only in current smokers.The hazardous effect of low HDL-C levels on lymphoma was significant only in never smokers (aHR, 2.01; 95% CI, 1.51-2.68). Hazardous effects of low HDL-C levels on leukemia were observed only in post-menopausal women (aHR, 2.94; 95% CI, 1.69-5.11).</p><p><strong>Conclusion: </strong>Low HDL-C levels were associated with a higher risk of leukemia and lymphoma, with discrepancies based on smoking and menopausal status.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"94-105"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular Pathways in Diabetic Cardiomyopathy and the Role of Anti-hyperglycemic Drugs Beyond Their Glucose Lowering Effect.","authors":"Jie-Eun Lee, Byung Gyu Kim, Jong Chul Won","doi":"10.12997/jla.2025.14.1.54","DOIUrl":"10.12997/jla.2025.14.1.54","url":null,"abstract":"<p><p>Epidemiological evidence has shown that diabetes is associated with overt heart failure (HF) and worse clinical outcomes. However, the presence of a distinct primary diabetic cardiomyopathy (DCM) has not been easy to prove because the association between diabetes and HF is confounded by hypertension, obesity, microvascular dysfunction, and autonomic neuropathy. In addition, the molecular mechanisms underlying DCM are not yet fully understood, DCM usually remains asymptomatic in the early stage, and no specific biomarkers have been identified. Nonetheless, several mechanistic associations at the systemic, cardiac, and cellular/molecular levels explain different aspects of myocardial dysfunction, including impaired cardiac relaxation, compliance, and contractility. In this review, we focus on recent clinical and preclinical advances in our understanding of the molecular mechanisms of DCM and the role of anti-hyperglycemic agents in preventing DCM beyond their glucose lowering effect.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"54-76"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fernando Bril, Gabriela Berg, Magali Barchuk, Juan Patricio Nogueira
{"title":"Practical Approaches to Managing Dyslipidemia in Patients With Metabolic Dysfunction-Associated Steatotic Liver Disease.","authors":"Fernando Bril, Gabriela Berg, Magali Barchuk, Juan Patricio Nogueira","doi":"10.12997/jla.2025.14.1.5","DOIUrl":"10.12997/jla.2025.14.1.5","url":null,"abstract":"<p><p>Dyslipidemia is a major risk factor for cardiovascular disease, and its impact may be exacerbated when accompanied by metabolic dysfunction-associated steatotic liver disease (MASLD). The simultaneous management of these conditions poses multiple challenges for healthcare providers. Insulin resistance has been implicated in the pathogenesis of both dyslipidemia and MASLD, necessitating a holistic approach to managing dyslipidemia, glucose levels, body weight, and MASLD. This review explores the intricate pathophysiological relationship between MASLD and dyslipidemia. It also examines current guidance regarding the use of lipid-lowering agents (including statins, ezetimibe, fibrates, omega-3 polyunsaturated fatty acids, and proprotein convertase subtilisin/kexin type 9 inhibitors) as well as glucose-lowering medications (such as pioglitazone, glucagon-like peptide-1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors) in patients with MASLD, with or without metabolic dysfunction-associated steatohepatitis (MASH), and dyslipidemia. Additionally, the review addresses the potential of emerging drugs to concurrently target both MASLD/MASH and dyslipidemia. Our hope is that a deeper understanding of the mechanisms underlying MASLD and dyslipidemia may assist clinicians in the management of these complex cases.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"5-29"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Response to Letter Regarding Article, Statins Ticagrelor and Rhabdomyolysis: A Coincidence or a Drug Interaction?","authors":"Jai Bharat Sharma, Ramesh Patel","doi":"10.12997/jla.2025.14.1.130","DOIUrl":"10.12997/jla.2025.14.1.130","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"130-131"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"<i>Journal of Lipid and Atherosclerosis</i> Update 2025.","authors":"Ji Hye Heo, In-Kyung Jeong","doi":"10.12997/jla.2025.14.1.3","DOIUrl":"10.12997/jla.2025.14.1.3","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"3-4"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Letter by Isa Ardahanli Regarding Article, Statins Ticagrelor and Rhabdomyolysis: A Coincidence or a Drug Interaction?","authors":"Isa Ardahanli, Murat Ozmen","doi":"10.12997/jla.2025.14.1.128","DOIUrl":"10.12997/jla.2025.14.1.128","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"128-129"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Corrigendum to Previously Published Articles.","authors":"","doi":"10.12997/jla.2025.14.1.132","DOIUrl":"https://doi.org/10.12997/jla.2025.14.1.132","url":null,"abstract":"<p><p>[This corrects the article on p. 61 in vol. 13, PMID: 38299164.][This corrects the article on p. 89 in vol. 13, PMID: 38826182.][This corrects the article on p. 338 in vol. 13, PMID: 39355400.][This corrects the article on p. 348 in vol. 13, PMID: 39355402.].</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"14 1","pages":"132-133"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11791420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic Vaccines and Nucleic Acid Drugs for Cardiovascular Disease.","authors":"Hironori Nakagami, Hiroki Hayashi, Ryuichi Morishita","doi":"10.12997/jla.2024.13.3.328","DOIUrl":"10.12997/jla.2024.13.3.328","url":null,"abstract":"<p><p>To combat the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), novel vaccine modalities, such as messenger RNA vaccines, were rapidly developed and have shown high efficacy. This new vaccine technology, underpinned by intensive immunological analysis, is now being applied to the production of other vaccines. For over 10 years, we have been developing therapeutic vaccines for non-infectious diseases. The epitope vaccine approach, which combines a B-cell epitope with exogenous T-cell epitopes presented through major histocompatibility complex molecules, has been proposed to induce antibody production. This vaccine type is designed to efficiently induce a blocking antibody response against the self-antigen without activating cytotoxic T cells. If therapeutic vaccines become established as treatment options for conditions such as hypertension or dyslipidemia, their administration-potentially only a few times per year-could replace the need for daily medication. Nucleic acid drugs, including small interfering RNA and antisense oligonucleotides, have recently received attention as long-term agonists, similar to vaccines. Therefore, therapeutic vaccines or nucleic acid drugs could represent a novel strategy for controlling the progression of cardiovascular diseases. It is hoped that the accumulation of immunological findings and advances in vaccine technology will provide valuable insights into the development of vaccines for treating cardiovascular diseases.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"328-337"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hoyoun Won, Jae Hyun Bae, Hyunjung Lim, Minji Kang, Minjoo Kim, Sang-Hak Lee
{"title":"2024 KSoLA Consensus on Secondary Dyslipidemia.","authors":"Hoyoun Won, Jae Hyun Bae, Hyunjung Lim, Minji Kang, Minjoo Kim, Sang-Hak Lee","doi":"10.12997/jla.2024.13.3.215","DOIUrl":"10.12997/jla.2024.13.3.215","url":null,"abstract":"<p><p>Elevated blood cholesterol and triglyceride levels induced by secondary causes are frequently observed. The identification and appropriate handling of these causes are essential for secondary dyslipidemia treatment. Major secondary causes of hypercholesterolemia and hypertriglyceridemia include an unhealthy diet, diseases and metabolic conditions affecting lipid levels, and therapeutic side effects. It is imperative to correct secondary causes prior to initiating conventional lipid-lowering therapy. Guideline-based lipid therapy can then be administered based on the subsequent lipid levels.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"215-231"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Extracellular Vesicles as Mediators in Atherosclerotic Cardiovascular Disease.","authors":"Lucia Zisser, Christoph J Binder","doi":"10.12997/jla.2024.13.3.232","DOIUrl":"10.12997/jla.2024.13.3.232","url":null,"abstract":"<p><p>Atherosclerosis is a chronic inflammatory disease of the arterial intima, characterized by accumulation of lipoproteins and accompanying inflammation, leading to the formation of plaques that eventually trigger occlusive thrombotic events, such as myocardial infarction and ischemic stroke. Although many aspects of plaque development have been elucidated, the role of extracellular vesicles (EVs), which are lipid bilayer-delimited vesicles released by cells as mediators of intercellular communication, has only recently come into focus of atherosclerosis research. EVs comprise several subtypes that may be differentiated by their size, mode of biogenesis, or surface marker expression and cargo. The functional effects of EVs in atherosclerosis depend on their cellular origin and the specific pathophysiological context. EVs have been suggested to play a role in all stages of plaque formation. In this review, we highlight the known mechanisms by which EVs modulate atherogenesis and outline current limitations and challenges in the field.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"232-261"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}