{"title":"Journal Metrics and Statistics.","authors":"Hyun Kang","doi":"10.12997/jla.2023.12.1.87","DOIUrl":"https://doi.org/10.12997/jla.2023.12.1.87","url":null,"abstract":"The number of total citations continuously increased. An estimated impact factor in Web of Science achieved a rising Journal Citation Reports (JCR) impact factor of 3.71(estimated value at December 1st, 2022), which corresponds to Journal Impact Factor Quartile 2 (Q2) in Biochemical Research Methods category, Quartile 3 (Q3) in Endocrinology & Metabolism category and Q3 in Peripheral Vascular Disease category (values are compared with JCR2022). In addition, the CiteScore Tracker 2022 (last updated on December 6th, 2022, available from: https://www.scopus.com/sourceid/21101032315) calculated by Scopus was 4.3 (342 citations to date/145 documents 2018 to date). This is a substantial increase compared with the 1.9 from the CiteScore Tracker 2021, in which the journal ranked 38th percentile in Internal Medicine category, 36th percentile in Cardiology and Cardiovascular Medicine category and 29th percentile in Endocrinology, Diabetes and Metabolism category. This is an unprecedented pace of development. J Lipid Atheroscler. 2023 Jan;12(1):87 https://doi.org/10.12997/jla.2023.12.1.87 pISSN 2287-2892·eISSN 2288-2561","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"12 1","pages":"87"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8e/bc/jla-12-87.PMC9884552.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10742589","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":"New Therapeutic Approaches to the Treatment of Dyslipidemia 1: ApoC-III and ANGPTL3.","authors":"Ji Yoon Kim, Nam Hoon Kim","doi":"10.12997/jla.2023.12.1.23","DOIUrl":"https://doi.org/10.12997/jla.2023.12.1.23","url":null,"abstract":"<p><p>Low-density lipoprotein cholesterol (LDL-C)-lowering therapy that increases LDL receptor expression in several ways robustly reduces the risk of atherosclerotic cardiovascular disease (CVD). However, a substantial risk of CVD still remains after intensive LDL-C reduction, which requires new treatment modalities for dyslipidemia and cardiovascular risk management. Triglycerides (TGs) and triglyceride-rich lipoproteins (TRLs) have received attention as indicators of residual cardiovascular risk and as direct causal factors for atherosclerosis and CVDs. Advances in understanding TG and TRL metabolism and their association with clinically evident CVDs have led to the development of novel therapeutic targets, including apolipoprotein C-III (apoC-III) and angiopoietin-like protein 3 (ANGPTL3). Genetic association studies have indicated that both apoC-III and ANGPTL3 play a causal role in the development of atherosclerotic CVD. Both molecules contribute to lipid dysregulation and atherosclerosis primarily by inhibiting lipoprotein lipase; however, recent evidence has shown that novel pathways exist in relation to their lipid-modifying activities. Notably, recent progress in therapeutic approaches, such as monoclonal antibodies or antisense oligonucleotides, has led to several novel therapeutics targeting apoC-III and ANGPTL3. This review summarized the recent updates and discussions related to apoC-III and ANGPTL3 expression.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"12 1","pages":"23-36"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e6/b0/jla-12-23.PMC9884553.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10679267","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}
Seyed Amirhossein Tabatabaei Dakhili, Amanda A Greenwell, John R Ussher
{"title":"Pyruvate Dehydrogenase Complex and Glucose Oxidation as a Therapeutic Target in Diabetic Heart Disease.","authors":"Seyed Amirhossein Tabatabaei Dakhili, Amanda A Greenwell, John R Ussher","doi":"10.12997/jla.2023.12.1.47","DOIUrl":"https://doi.org/10.12997/jla.2023.12.1.47","url":null,"abstract":"<p><p>Diabetic cardiomyopathy was originally described as the presence of ventricular dysfunction in the absence of coronary artery disease and/or hypertension. It is characterized by diastolic dysfunction and is more prevalent in people with diabetes than originally realized, leading to the suggestion in the field that it simply be referred to as diabetic heart disease. While there are currently no approved therapies for diabetic heart disease, a multitude of studies clearly demonstrate that it is characterized by several disturbances in myocardial energy metabolism. One of the most prominent changes in myocardial energy metabolism in diabetes is a robust impairment in glucose oxidation. Herein we will describe the mechanisms responsible for the diabetes-induced decline in myocardial glucose oxidation, and the pharmacological approaches that have been pursued to correct this metabolic disorder. With surmounting evidence that stimulating myocardial glucose oxidation can alleviate diastolic dysfunction and other pathologies associated with diabetic heart disease, this may also represent a novel strategy for decreasing the prevalence of heart failure with preserved ejection fraction in the diabetic population.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"12 1","pages":"47-57"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e9/01/jla-12-47.PMC9884548.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10688898","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":"Deep Appreciation to Our Reviewers in the Past Year 2022.","authors":"Hyun Kang","doi":"10.12997/jla.2023.12.1.2","DOIUrl":"https://doi.org/10.12997/jla.2023.12.1.2","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"12 1","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7b/91/jla-12-2.PMC9884556.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10742590","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":"Message From the New Editor-in-Chief.","authors":"Hyun Kang","doi":"10.12997/jla.2023.12.1.1","DOIUrl":"https://doi.org/10.12997/jla.2023.12.1.1","url":null,"abstract":"","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"12 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c9/11/jla-12-1.PMC9884551.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10742588","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}
Heekyoung Jeong, Kyungdo Han, Soon Jib Yoo, Mee Kyoung Kim
{"title":"Low-Density Lipoprotein Cholesterol Level, Statin Use and Myocardial Infarction Risk in Young Adults.","authors":"Heekyoung Jeong, Kyungdo Han, Soon Jib Yoo, Mee Kyoung Kim","doi":"10.12997/jla.2022.11.3.288","DOIUrl":"https://doi.org/10.12997/jla.2022.11.3.288","url":null,"abstract":"<p><strong>Objective: </strong>The consequences of blood lipid abnormalities for cardiovascular disease risk in young adults is unclear. Optimal lipid levels may also vary depending on whether a statin drug is taken. It aimed to determine whether the optimal lipid levels in young adults differ depending on statin use.</p><p><strong>Methods: </strong>Using a nationally representative database from the Korean National Health Insurance System, 6,350,400 participants aged 20-39 years who underwent a health examination between 2009-2012 were followed through to 2018. The primary outcome was incident myocardial infarction (MI). We assessed the associations between prespecified lipid levels and MI risk according to statin use.</p><p><strong>Results: </strong>Among participants not taking statins, low-density lipoprotein cholesterol (LDL-C) levels ≥120 mg/dL were significantly associated with MI risk (hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.27-1.40) compared with statin nonusers with LDL-C <80 mg/dL. Statin users with LDL-C categories <80, 80-100, 100-120, and ≥120 mg/dL all had significantly higher MI risk compared with statin nonusers with LDL-C <80 mg/dL; these HRs (95% CIs) were 1.66 (1.39-1.99), 1.68 (1.36-2.09), 1.63 (1.31-2.02), and 2.32 (2.07-2.60), respectively.</p><p><strong>Conclusion: </strong>Young adults taking statins have an increased MI risk compared with statin nonusers, even when they have similar LDL-C levels. Specific lipid targets may need to differ depending on statin use.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"11 3","pages":"288-298"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/e9/fe/jla-11-288.PMC9515733.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33497681","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":"Shinjulactone A Blocks Vascular Inflammation and the Endothelial-Mesenchymal Transition.","authors":"Ye-Eun Jang, Jenita Immanuel, Jin-Ri Lee, Yu-Jin Jang, Yun Ju Kwon, Hyun Sook Kwon, Jung-Woog Shin, Sanguk Yun","doi":"10.12997/jla.2022.11.3.272","DOIUrl":"https://doi.org/10.12997/jla.2022.11.3.272","url":null,"abstract":"<p><strong>Objective: </strong>The endothelial inflammatory response plays an important role in atherogenesis by inducing nuclear factor (NF)κB-dependent cell adhesion molecule expression and monocyte recruitment. Here, we screened for natural ligands and investigated the ability of shinjulactone A to inhibit interleukin-1β (IL-1β)-induced endothelial inflammatory signaling.</p><p><strong>Methods: </strong>The natural compound library included 880 single compounds isolated from medicinal plants by the Korean Medicinal Material Bank. Primary endothelial cells were pretreated with single compounds before stimulation with IL-1β to induce endothelial inflammation. Endothelial inflammation was measured by assaying NFκB activation and monocyte adhesion. The endothelial-mesenchymal transition (EndMT) was evaluated using cell type-specific marker protein expression and morphology.</p><p><strong>Results: </strong>Shinjulactone A was identified as an efficient blocker of IL-1β -induced NFκB activation, with a half-maximal inhibitory concentration of approximately 1 µM, and monocyte recruitment in endothelial cells. However, it did not affect lipopolysaccharide-induced NFκB activation in macrophages. Compared to Bay 11-782, a well-known NFκB inhibitor that shows considerable cytotoxicity during long-term treatment, shinjulactone A did not affect endothelial cell viability. Furthermore, it also significantly inhibited the EndMT, which is known to promote atherosclerosis and plaque instability.</p><p><strong>Conclusion: </strong>We suggest that shinjulactone A may be an effective and safe drug candidate for atherosclerosis because it targets and inhibits both endothelial inflammation and the EndMT, without impairing NFκB-dependent innate immunity in macrophages.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"11 3","pages":"272-279"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/34/ac/jla-11-272.PMC9515731.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33496072","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}
Chan Joo Lee, Sanghyun Park, Kyungdo Han, Sang-Hak Lee
{"title":"Impact of Severe Hypercholesterolemia on Cardiovascular Risk in Individuals With or Without Diabetes Mellitus.","authors":"Chan Joo Lee, Sanghyun Park, Kyungdo Han, Sang-Hak Lee","doi":"10.12997/jla.2022.11.3.299","DOIUrl":"https://doi.org/10.12997/jla.2022.11.3.299","url":null,"abstract":"<p><strong>Objective: </strong>The aim of the current study was to investigate whether the impact of low-density lipoprotein-cholesterol (LDL-C) levels on cardiovascular risk is different between individuals with severe hypercholesterolemia and diabetes mellitus (DM) and those without DM.</p><p><strong>Methods: </strong>This study used the database of a National Health Insurance Service cohort of Korea. Among individuals who underwent health check-up, 2,261,332 were included and categorized into 3 groups with severe hypercholesterolemia, >260, 225-259, and 190-224 mg/dL groups, and a control group (<160 mg/dL). Risks of composite events (myocardial infarction [MI], coronary revascularization, and ischemic stroke) and total mortality were analyzed, according to the presence of DM.</p><p><strong>Results: </strong>Of the study population, 5.2% had DM. During median follow-up of 6.1 years, the rates of composite events (/1,000 person-year) in non-DM and DM subjects were up to 5.66 and 8.92, respectively. Adjusted hazard ratios (aHRs) of the composite events ranged up to 3.11 and 1.44 in non-DM and DM groups, respectively (<i>p</i><0.0001 between LDL-C categories in both groups). Dependency of aHR on LDL-C levels was more prominent in the non-DM group. aHRs of MI and coronary revascularization showed similar tendency to the composite events. Although aHRs of ischemic stroke (<i>p</i><0.0001) and total mortality (<i>p</i>=0.002) were different according to LDL-C categories in the non-DM group, these relations were not observed in DM group.</p><p><strong>Conclusion: </strong>Although individuals with severe hypercholesterolemia had high cardiovascular risk when DM was present, the impact of LDL-C on the risk was attenuated in this population.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"11 3","pages":"299-307"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/80/67/jla-11-299.PMC9515734.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33497682","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}
Ki-Woong Nam, Hyung-Min Kwon, Jin-Ho Park, Hyuktae Kwon
{"title":"The Atherogenic Index of Plasma is Associated With Cerebral Small Vessel Disease: A Cross-Sectional Study.","authors":"Ki-Woong Nam, Hyung-Min Kwon, Jin-Ho Park, Hyuktae Kwon","doi":"10.12997/jla.2022.11.3.262","DOIUrl":"https://doi.org/10.12997/jla.2022.11.3.262","url":null,"abstract":"<p><strong>Objective: </strong>Recently, the lipid profile of atherogenic dyslipidemia has become important in cerebrovascular diseases. Atherogenic index of plasma (AIP), an index that reflects this lipid profile as a single number, has been proposed, but there are still few related studies in cerebrovascular disease. In this study, we evaluated the relationship between AIP and cerebral small vessel disease (cSVD) in health check-up participants.</p><p><strong>Methods: </strong>We assessed consecutive health check-ups participants between 2006 and 2013. cSVD was measured including the following three subtypes: white matter hyperintensity (WMH), lacuens, and cerebral microbleeds (CMBs). WMH quantitatively measured the volume, and lacunes and CMBs qualitatively evaluated the presence. AIP was calculated according to the following formula based on blood test results: AIP=log [triglyceride (mg/dL)/high-density lipoprotein cholesterol (mg/dL)].</p><p><strong>Results: </strong>A total of 3,170 participants were evaluated (mean age: 56.5 years, male sex: 53.8%). In multivariable linear regression analysis, AIP (<i>β</i>=0.129, 95% confidence interval [CI]=0.003-0.255) was associated with WMH. Age, hypertension, diabetes, lipid-lowering agents, and intracranial atherosclerosis were also associated with WMH volume. In multivariable logistic regression analysis, AIP (adjusted odds ratio=1.72 1.79, 95% CI=1.03-2.90) showed close association with lacunes. Age and intracranial atherosclerosis were also related to lacunes. CMBs did not show a statistically significant association with AIP.</p><p><strong>Conclusion: </strong>High AIP was associated with cSVD in health check-up participants. Since this close relationship was only seen in WMH and lacunes, these subtypes may have arisen from a more atherosclerosis-related pathology.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"11 3","pages":"262-271"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c5/e2/jla-11-262.PMC9515737.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33497683","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":"A New Modality in Dyslipidemia Treatment: Antisense Oligonucleotide Therapy.","authors":"Kyuho Kim, Sung Hee Choi","doi":"10.12997/jla.2022.11.3.250","DOIUrl":"https://doi.org/10.12997/jla.2022.11.3.250","url":null,"abstract":"<p><p>There are unmet needs for pharmacologic agents beyond current medications, such as statins, to effectively lower low-density lipoprotein cholesterol levels to target goals, especially in patients with very high or extremely high risk. Pharmacological targeting of mRNA represents an emerging, innovative approach with the potential to expand upon current therapies. In RNA-targeted therapeutics, a novel approach is the use of chemically modified oligonucleotides to inhibit the production of target proteins at their sites of gene coding. There are two main classes of RNA-targeted therapeutics: single-stranded antisense oligonucleotides (ASOs) and double-stranded small inhibiting RNAs. ASOs are synthetic molecules with a length of 15-30 nucleotides that are designed specifically to bind to a target mRNA in a sequence-specific manner. Using these agents to inhibit the translation of key regulatory proteins, such as apolipoprotein CIII, apolipoprotein(a), and angiopoietin-like protein 3, has demonstrated treatment efficacy for dyslipidemia. Many cardiovascular outcome trials with ASOs are ongoing. As clinicians, we must carefully monitor the long-term safety and efficacy of this new modality through large clinical trials in the future.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"11 3","pages":"250-261"},"PeriodicalIF":0.0,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3a/e7/jla-11-250.PMC9515732.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33497685","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}