Journal of Lipid and Atherosclerosis最新文献

{"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}

{"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":"Comparison of Multiple Equations for Low-Density Lipoprotein Cholesterol Calculation Against the Direct Homogeneous Method.","authors":"Rawaa E K Alsadig, Adel N Morsi","doi":"10.12997/jla.2024.13.3.348","DOIUrl":"10.12997/jla.2024.13.3.348","url":null,"abstract":"<p><strong>Objective: </strong>Several equations have been proposed as alternatives for the reference method of measuring low-density lipoprotein cholesterol (LDL-C). This study aimed to evaluate these alternatives in comparison to the homogeneous method and validate their clinical utility.</p><p><strong>Methods: </strong>Data on the lipid profiles of 1,006 Sudanese individuals were analyzed. The paired t-test was used to compare the results of direct and calculated LDL-C. Bland-Altman plots were used to demonstrate the differences between the measured and calculated LDL-C against the mean values. Linear regression was conducted, using the correlation coefficient (<i>r</i>) to quantify the relationship between methods. The bias between measured and calculated LDL-C was compared to the National Cholesterol Education Program Laboratory Standardization Panel criteria (i.e., accuracy within ±4% of expected values).</p><p><strong>Results: </strong>The Martin and Anandaraja equations showed no significant difference compared to directly measured LDL-C (<i>p</i>>0.05). The DeLong equation indicated an insignificant difference only with a 99% confidence interval (<i>p</i>>0.01). The Martin, DeLong, and Teerakanchana equations exhibited the smallest limits of agreement, with data points concentrated closely around the mean difference line. Linear regression analysis revealed strong positive correlations (<i>r</i>>0.8) for most equations, except for the Ahmadi equation. The DeLong, Rao, and Martin equations demonstrated superior performance for LDL cutoff points (bias within ± 4%). The DeLong formula also showed superior performance at different lipid levels, closely followed by the Martin equation (bias within ±4%).</p><p><strong>Conclusion: </strong>The DeLong and Martin equations outperformed others, such as the widely used Friedewald equation, in calculating LDL-C. Further validation studies are needed.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"348-357"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361561","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}

{"title":"Emerging Circulating Biomarkers for Enhanced Cardiovascular Risk Prediction.","authors":"Da Young Lee","doi":"10.12997/jla.2024.13.3.262","DOIUrl":"10.12997/jla.2024.13.3.262","url":null,"abstract":"<p><p>Cardiovascular disease (CVD) continues to be the primary cause of mortality worldwide, underscoring the importance of identifying additional cardiovascular risk factors. The consensus is that lipid levels alone do not fully reflect the status of atherosclerosis, thus necessitating extensive research on cardiovascular biomarkers. This review encompasses a wide spectrum of methodologies for identifying novel risk factors or biomarkers for CVD. Inflammation, oxidative stress, plaque instability, cardiac remodeling, and fibrosis play pivotal roles in CVD pathogenesis. We introduce and discuss several promising biomarkers-namely, osteocalcin, angiogenin, lipoprotein-associated phospholipase A2, growth differentiation factor 15, galectin-3, growth stimulation expressed gene 2, and microRNAs, all of which have potential implications in the assessment and management of cardiovascular risk.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"262-279"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361562","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":"The Effects of Anti-thyroid Drugs on Lipoproteins and Insulin Resistance in Graves' Disease: A Randomized Clinical Trial.","authors":"Wismandari Wisnu, Idrus Alwi, Nafrialdi Nafrialdi, Tjokorda Gde Dalem Pemayun, Nico Iswanto Pantoro, Calysta Nadya Wijaya, Dicky Levenus Tahapary, Tri Juli Edi Tarigan, Imam Subekti","doi":"10.12997/jla.2024.13.3.358","DOIUrl":"10.12997/jla.2024.13.3.358","url":null,"abstract":"<p><strong>Objective: </strong>Graves' disease (GD) is characterized by thyroid overactivity. Anti-thyroid drugs (ATDs), such as propylthiouracil (PTU) and methimazole (MMI), are commonly used for GD treatment, and studies have suggested a link between these drugs and elevated lipoprotein levels. However, data on their effects on lipoproteins, insulin resistance, or low-density lipoprotein receptor (LDL-R) levels are lacking, both in Indonesia and in other countries. This study investigated changes in lipoproteins, LDL-R, and insulin resistance markers with ATD treatment.</p><p><strong>Methods: </strong>This study is a secondary analysis of a randomized clinical trial entitled \"The Differential Effects of Propylthiouracil and Methimazole as Graves' Disease Treatment on Vascular Atherosclerosis Markers\" conducted in Jakarta, Indonesia. Thirty-seven newly diagnosed GD patients received MMI or PTU for 3 months.</p><p><strong>Results: </strong>After 3 months of ATD treatment, LDL-R levels significantly decreased compared to baseline (197 vs. 144 ng/mL, <i>p</i><0.001), while most lipoproteins, including TC, LDL-C, HDL-C, non-HDL-C, the cholesterol ratio, and the LDL-C/HDL-C ratio, increased. Unexpectedly, neither the PTU nor MMI groups showed an increased dyslipidemia prevalence. Although body mass index increased significantly and fasting plasma glucose decreased slightly, no significant post-treatment change in insulin resistance was observed. The study received ethical approval from the Ethics Committee of the Faculty of Medicine, Universitas Indonesia (ref KET-784/UN.2.F1/ETIK/PPM.00.02/2019) and was registered on clinicaltrials.gov (NCT05118542).</p><p><strong>Conclusion: </strong>ATD treatment for GD led to a significant increase in total cholesterol, LDL-cholesterol, and high-density lipoprotein-cholesterol levels, along with a reduction in LDL-R levels. Both PTU and MMI showed similar effects. These findings provide valuable insights into the effects of ATDs on lipoproteins and insulin resistance in GD patients.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov Identifier: NCT05118542.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"358-370"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439756/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361567","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":"Adherence to Dietary Patterns and Cardiovascular Disease Risk: A Cross-Sectional Study of Total Carotid Plaque Area in Argentina.","authors":"Mariana N Carrillo, Matias Garribia, Luis Armando, Akinwunmi Oluwaseun Adeoye, Nestor H Garcia, Sonia E Muñoz","doi":"10.12997/jla.2024.13.3.338","DOIUrl":"10.12997/jla.2024.13.3.338","url":null,"abstract":"<p><strong>Objective: </strong>Assessing subclinical atherosclerosis (sAT) is crucial for preventing cardiovascular disease. The Mediterranean diet is considered the gold standard for cardiovascular protection, but cultural and economic barriers can hinder adherence to it. The prudent dietary pattern (DP) has been associated with protective effects against chronic diseases. However, its impact on primary cardiovascular prevention remains uncertain. This study examined adherence to various DPs and their effect on sAT, measured by total carotid plaque area (TPA).</p><p><strong>Methods: </strong>This cross-sectional study included 116 adults enrolled in a cardiovascular prevention program. Demographic, clinical, laboratory, and TPA data were collected. Adherence to DPs was assessed using a food frequency questionnaire. Participants were categorized according to their adherence to 4 mutually exclusive DPs: prudent, traditional, sweet, and mixed. Generalized linear models were used to assess the effect of DPs on TPA, adjusting for relevant cardiovascular variables.</p><p><strong>Results: </strong>The traditional, sweet, and mixed DPs were associated with higher TPA values than the prudent DP, with medians (interquartile range) of 27 (99), 39 (49), 27.5 (58), and 0 (36) mm², respectively. Gamma regression analysis found that the beta exponents for the traditional, sweet, and mixed DPs versus the prudent DP were 3.78 (<i>p</i>=0.046); 3.73 (<i>p</i>=0.013), and 2.20 (<i>p</i>=0.072), respectively. Systolic blood pressure values were higher for the sweet and mixed DPs than for the prudent DP (133.9±11.7; 132.5±13.9 and 122.7±8.8 mmHg, respectively; <i>p</i><0.05).</p><p><strong>Conclusion: </strong>These findings underscore the importance of additional research and targeted interventions to promote healthier DPs to promote improvements in cardiovascular health.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"338-347"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439755/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361660","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":"Mendelian Randomization Studies in Atherosclerotic Cardiovascular Diseases.","authors":"Dai Sik Ko, Yun Hak Kim","doi":"10.12997/jla.2024.13.3.280","DOIUrl":"10.12997/jla.2024.13.3.280","url":null,"abstract":"<p><p>This review aimed to highlight the pivotal role of Mendelian randomization (MR) in advancing atherosclerotic cardiovascular disease (ASCVD) research-a field often hindered by the complexities and limitations of traditional studies. MR, which uses genetic variants as instrumental variables, provides a robust mechanism for inferring causality, offering insights untainted by the confounding factors and biases often prevalent in observational and randomized controlled trials. We explored the significant contributions of MR for elucidating the causal relationship between low-density lipoprotein cholesterol and ASCVD, and analyzed its assumptions and methodological nuances. We discussed issues surrounding instrumental variable selection, pleiotropy, and ethical considerations, in an effort to offer a balanced and insightful analysis. We highlighted the promising integration of MR with emerging technologies and global data sharing, as well as its potential to drive personalized medicine. This review provided a concise yet comprehensive journey into MR's transformative impact on ASCVD research, offering a blend of current insights and challenges, in addition to future prospects. We aimed to serve a valuable resource for those seeking to navigate the intricate pathways of causality and intervention in ASCVD, to aid the development of enhanced understanding and targeted treatment strategies in the future.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"280-291"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361564","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":"Nrf2 Connects Cellular Autophagy and Vascular Senescence in Atherosclerosis: A Mini-Review.","authors":"Kai Wen Wai, Liang Ee Low, Bey Hing Goh, Wei Hsum Yap","doi":"10.12997/jla.2024.13.3.292","DOIUrl":"10.12997/jla.2024.13.3.292","url":null,"abstract":"<p><p>Nuclear factor erythroid 2-related factor 2 (Nrf2), a transcriptional factor that maintains intracellular redox equilibrium, modulates the expression of antioxidant genes, scavenger receptors, and cholesterol efflux transporters, all of which contribute significantly to foam cell development and plaque formation. Nrf2 has recently emerged as a key regulator that connects autophagy and vascular senescence in atherosclerosis. Autophagy, a cellular mechanism involved in the breakdown and recycling of damaged proteins and organelles, and cellular senescence, a state of irreversible growth arrest, are both processes implicated in the pathogenesis of atherosclerosis. The intricate interplay of these processes has received increasing attention, shedding light on their cumulative role in driving the development of atherosclerosis. Recent studies have revealed that Nrf2 plays a critical role in mediating autophagy and senescence in atherosclerosis progression. Nrf2 activation promotes autophagy, which increases lipid clearance and prevents the development of foam cells. Meanwhile, the activation of Nrf2 also inhibits cellular senescence by regulating the expression of senescence markers to preserve cellular homeostasis and function and delay the progression of atherosclerosis. This review provides an overview of the molecular mechanisms through which Nrf2 connects cellular autophagy and vascular senescence in atherosclerosis. Understanding these mechanisms can provide insights into potential therapeutic strategies targeting Nrf2 to modulate cellular autophagy and vascular senescence, thereby preventing the progression of atherosclerosis.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"292-305"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361565","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":"Targeting Mitochondrial Dysfunction for the Prevention and Treatment of Metabolic Disease by Bioactive Food Components.","authors":"Mi-Bo Kim, Jaeeun Lee, Ji-Young Lee","doi":"10.12997/jla.2024.13.3.306","DOIUrl":"10.12997/jla.2024.13.3.306","url":null,"abstract":"<p><p>Dysfunctional mitochondria have been linked to the pathogenesis of obesity-associated metabolic diseases. Excessive energy intake impairs mitochondrial biogenesis and function, decreasing adenosine-5'-triphosphate production and negatively impacting metabolically active tissues such as adipose tissue, skeletal muscle, and the liver. Compromised mitochondrial function disturbs lipid metabolism and increases reactive oxygen species production in these tissues, contributing to the development of insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease. Recent studies have demonstrated the therapeutic potential of bioactive food components, such as resveratrol, quercetin, coenzyme Q10, curcumin, and astaxanthin, by enhancing mitochondrial function. This review provides an overview of the current understanding of how these bioactive compounds ameliorate mitochondrial dysfunction to mitigate obesity-associated metabolic diseases.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"13 3","pages":"306-327"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361566","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}