Journal of Lipid and Atherosclerosis最新文献

{"title":"Frequency of Low HDL Cholesterol and the Dose-Dependent Risk of Type 2 Diabetes: A Longitudinal Cohort Study.","authors":"Min-Kyung Lee, Jung Heo, Jae-Hyuk Lee, Bongsung Kim, Kyungdo Han","doi":"10.12997/jla.2026.15.3.509","DOIUrl":"10.12997/jla.2026.15.3.509","url":null,"abstract":"<p><strong>Objective: </strong>Although low high-density lipoprotein cholesterol (HDL-C) is an established risk factor for type 2 diabetes (T2D), most studies have relied on single-point measurements. We investigated whether persistent low HDL-C levels were associated with an increased risk of incident T2D in young adults.</p><p><strong>Methods: </strong>We included 1,840,251 individuals from the Korean National Health Insurance Service database (2009-2012) who underwent 4 consecutive annual health examinations. Participants were categorized into 5 groups according to the frequency of low HDL-C exposure (0-4 times; <40 mg/dL in men and <50 mg/dL in women). The risk of incident T2D was assessed using multivariable Cox proportional hazards models over a mean follow-up of 6.5 years.</p><p><strong>Results: </strong>The risk of T2D increased significantly with increasing frequency of low HDL-C exposure (<i>p</i><0.0001). The hazard ratios (95% confidence intervals [CIs]) for incident T2D were 1.472 (95% CI, 1.433-1.512), 1.786 (95% CI, 1.730-1.844), 1.990 (95% CI, 1.919-2.063), and 2.021 (95% CI, 1.941-2.105) for the groups with low HDL-C exposure 1, 2, 3, and 4 times, respectively, compared with the 0-time group (<i>p</i> for trend <0.0001). Subgroup analyses revealed consistent associations across all strata, with stronger associations among participants aged <30 years, women, and those with body mass index <25 kg/m².</p><p><strong>Conclusion: </strong>A clear dose-response relationship was observed, indicating that cumulative exposure to low HDL-C levels was strongly associated with an increased risk of T2D. This association remained robust regardless of metabolic status, although it was more pronounced in younger adults, women, and non-obese individuals.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"509-518"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081049","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":"Statin Use and Site-Specific Cancer Risk: A Nationwide Cohort Study Using Korean Health Insurance Data.","authors":"Jihoon Seo, Jung Yoon Moon, Ye-Jee Kim, Hwa Jung Kim, Chang Hee Jung, Woo Je Lee, Yun Kyung Cho","doi":"10.12997/jla.2026.15.3.498","DOIUrl":"10.12997/jla.2026.15.3.498","url":null,"abstract":"<p><strong>Objective: </strong>Statins are used for cardiovascular prevention and may exert anticancer effects by modulating the mevalonate pathway and tumor microenvironment. However, population-based evidence in Koreans remains limited. This study evaluated the association between statin use and cancer risk using Korean nationwide health data.</p><p><strong>Methods: </strong>This population-based cohort study used the Korean National Health Insurance Service database. Individuals who underwent health screening in 2009-2010 were followed until 2019. Statin users referred to individuals prescribed statins for ≥6 months, whereas non-users had no statin exposure. Incident cancers were identified using International Classification of Diseases, 10th Revision, codes. Multivariable Cox proportional hazards models were used to estimate adjusted hazard ratios (aHRs).</p><p><strong>Results: </strong>Among 232,133 participants (67,064 statin users, 165,069 non-users), the incidence rate for all malignancies was 10.60 per 1,000 person-years (PY) in statin users and 10.18 per 1,000 PY in non-users. After adjusting for confounders, statin use was associated with a modest but significant reduction in overall cancer risk (aHR, 0.96; 95% confidence interval [CI], 0.93-1.00; <i>p</i>=0.031). Site-specific analyses demonstrated reduced risk of liver cancer (aHR, 0.52; 95% CI, 0.44-0.61; <i>p</i><0.001) among statin users. Conversely, thyroid cancer incidence was higher among statin users, and statin use was markedly associated with increased thyroid cancer risk (aHR, 1.19; 95% CI, 1.07-1.33; <i>p</i>=0.001).</p><p><strong>Conclusion: </strong>In this nationwide Korean cohort, statin use was associated with a reduced risk of liver cancer but a significantly increased risk of thyroid cancer. These findings suggest organ-specific effects of statins on carcinogenesis and warrant further mechanistic investigation.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"498-508"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620174/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081111","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":"Metabolic and Clinical Outcomes of Combined Pitavastatin and Valsartan Therapy in Patients With Acute Myocardial Infarction: A Multicenter Prospective Observational Study.","authors":"Kyung Hoon Cho, Young Joon Hong, Sang-Rok Lee, Jung-Sun Kim, Seung-Woon Rha, Jung Ho Heo, Jin-Man Cho, Seung-Jin Oh, Il-Soo Lee, Wang Soo Lee, Kyeong Ho Yun, Ki-Sik Kim, Myung Ho Jeong","doi":"10.12997/jla.2026.15.3.533","DOIUrl":"10.12997/jla.2026.15.3.533","url":null,"abstract":"<p><strong>Objective: </strong>We evaluated the efficacy and safety of combined pitavastatin and valsartan therapy in patients with acute myocardial infarction.</p><p><strong>Methods: </strong>This non-interventional, multicenter, prospective observational study included 836 patients receiving combined pitavastatin and valsartan (80 mg) with 48 weeks of follow-up. Co-primary outcomes were major adverse cardiovascular events (MACEs) and changes in metabolic profiles.</p><p><strong>Results: </strong>Among 698 patients (mean age 61.8±12.1 years; 81.4% male) treated with pitavastatin/valsartan 2/80 mg or 4/80 mg, 15 MACEs occurred at 48 weeks (15/698, 2.1%). The mean (standard deviation) changes in fasting blood glucose and glycated hemoglobin from baseline to 48 weeks were -11.4±45.0 mg/dL (<i>p</i>=0.467) and -0.17±0.29% (<i>p</i>=0.165) for the 2/80 mg group, and -7.9±46.2 mg/dL (<i>p</i>=0.043) and -0.06±1.07% (<i>p</i>=0.181) for the 4/80 mg group, respectively. The mean (standard deviation) reductions in low-density lipoprotein cholesterol from baseline to 48 weeks were -27.9±24.7 mg/dL (<i>p</i>=0.006) for 2/80 mg and -29.9±38.1 mg/dL (<i>p</i><0.001) for 4/80 mg. No serious adverse drug reactions were observed except for one case of chest pain in one patient.</p><p><strong>Conclusion: </strong>This multicenter, prospective observational study of 836 patients with acute myocardial infarction and 48-week follow-up demonstrated that combined pitavastatin and valsartan therapy was associated with a low incidence of MACEs and was not associated with unfavorable metabolic profiles, although it should be cautiously interpreted due to the lack of a control arm and missing substantial follow-up data.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"533-543"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081058","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":"Cardiovascular Risk Associated With General and Abdominal Obesity in Young Adults Without Traditional Risk Factors: A Korean Nationwide Cohort Study.","authors":"Jeen Hwa Lee, Mina Kim, Hoseob Kim, Yeon Jung Lee, Myung Soo Park, Sook Jin Lee, Seongwoo Han, Dae Young Cheon","doi":"10.12997/jla.2026.15.3.544","DOIUrl":"10.12997/jla.2026.15.3.544","url":null,"abstract":"<p><strong>Objective: </strong>Body mass index (BMI) is widely used to classify obesity but does not adequately characterize central adiposity. Waist-to-height ratio (WHtR) is a simple anthropometric marker of central obesity that may detect cardiovascular risk not captured by BMI. This study examined whether WHtR provides prognostic information beyond BMI for cardiovascular risk stratification in young adults.</p><p><strong>Methods: </strong>We analyzed 1,743,968 adults aged 30-39 years who underwent health screening through the 2009 Korean National Health Insurance Service program. Participants were classified into four groups according to BMI and WHtR: BMI <25 kg/m² and WHtR <0.5; BMI ≥25 kg/m² and WHtR <0.5; BMI <25 kg/m² and WHtR ≥0.5; and BMI ≥25 kg/m² and WHtR ≥0.5. The primary endpoint was a composite of myocardial infarction (MI), stroke, and cardiovascular death. Multivariable Cox proportional hazards models were used to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs).</p><p><strong>Results: </strong>During a median follow-up of 14.2 years, 37,120 participants (2.12%) experienced the composite outcome. After multivariable adjustment, participants with normal BMI but elevated WHtR (Group 3) had an increased risk compared with Group 1 (aHR, 1.171; 95% CI, 1.118-1.226), with a slightly higher point estimate than Group 2. A similar pattern was observed for MI, whereas stroke risk was more strongly associated with elevated BMI.</p><p><strong>Conclusion: </strong>Elevated WHtR was associated with increased risk of MI and the composite outcome among young adults with normal BMI. WHtR may provide information complementary to BMI for early cardiovascular risk stratification.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"544-554"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081085","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":"Optimal LDL-C Levels for Ischemic Stroke Prevention: A Neurologist's Perspective.","authors":"Wookjin Yang","doi":"10.12997/jla.2026.15.3.399","DOIUrl":"10.12997/jla.2026.15.3.399","url":null,"abstract":"<p><p>Low-density lipoprotein cholesterol (LDL-C) lowering is a central therapeutic strategy in atherosclerotic cardiovascular disease (ASCVD) and is also important for ischemic stroke. As outcome-driven evidence has accumulated, lipid management guidelines have progressively adopted more stringent LDL-C targets. Landmark trials of statins, ezetimibe, and proprotein convertase subtilisin/kexin type 9 inhibitors have shown consistent cardiovascular benefit across progressively lower achieved LDL-C levels in ASCVD. In the stroke field, randomized controlled trials, including Stroke Prevention by Aggressive Reduction in Cholesterol Levels and Treat Stroke to Target, have provided stroke-specific evidence supporting intensive LDL-C lowering for secondary prevention, particularly in patients with atherosclerotic stroke. Beyond its established role in long-term secondary prevention, emerging evidence suggests that intensive LDL-C lowering may also affect the early clinical course after ischemic stroke. Nevertheless, important knowledge gaps remain. Ischemic stroke is a heterogeneous disease with diverse etiologic mechanisms, including nonatherosclerotic subtypes such as small vessel occlusion and cardioembolism. Because evidence-based LDL-C targets for these populations remain poorly defined, current guidelines focus mainly on atherosclerotic stroke, leaving uncertainty regarding optimal lipid management in nonatherosclerotic stroke subtypes. Ongoing large-scale clinical trials specifically targeting these populations are expected to address this gap and to inform more tailored lipid-lowering strategies in stroke care. This review summarizes current evidence on LDL-C targets and lipid-lowering therapy in ischemic stroke and considers the implications for clinical practice and future research.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"399-410"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081081","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":"Familial Hypercholesterolemia in Latin America: Unmet Needs, Barriers, and Challenges.","authors":"Rodrigo Alonso, Pablo Corral","doi":"10.12997/jla.2026.15.3.458","DOIUrl":"10.12997/jla.2026.15.3.458","url":null,"abstract":"<p><p>Familial hypercholesterolemia (FH) is the most common monogenic disorder predisposing individuals to premature atherosclerotic cardiovascular disease. Despite an estimated prevalence of 1 in 250 individuals, FH remains largely underdiagnosed and undertreated across Latin America, where more than 2 million people are expected to be living with FH. Early identification and intensive lipid-lowering therapy substantially improve clinical outcomes; however, multiple structural, socioeconomic, and educational barriers continue to limit optimal care throughout the region. FH detection rates remain low, and screening strategies are implemented heterogeneously: while opportunistic screening is emerging in some settings, cascade screening remains underdeveloped, with the exception of pioneering programs in Brazil and Uruguay. Real-world data from regional registries consistently demonstrate poor attainment of low-density lipoprotein cholesterol targets, partly due to the predominant use of statin monotherapy. Strengthening clinical registries, expanding access to genetic testing, implementing structured cascade screening programs, and improving availability of effective lipid-lowering therapies are essential steps to reduce the clinical and public health burden of FH in Latin America.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"458-470"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081033","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":"Myosteatosis and Dyslipidemia: Linking Muscle Quality to Cardiometabolic Risk.","authors":"Jung Yoon Moon, Chang Hee Jung","doi":"10.12997/jla.2026.15.3.445","DOIUrl":"10.12997/jla.2026.15.3.445","url":null,"abstract":"<p><p>Myosteatosis, the pathological accumulation of ectopic fat within skeletal muscle, has emerged as a key indicator of impaired muscle quality and metabolic dysfunction. It encompasses intermuscular and intramuscular adipose tissue as well as intramyocellular lipid, which differ in anatomical location, assessment methodology, and metabolic role. This review provides an integrated overview of myosteatosis, focusing on its bidirectional relationship with dyslipidemia. Myosteatosis represents a metabolically active fat depot characterized by heightened lipolytic and pro-inflammatory activity. It serves not only as an energy substrate for muscle contraction but also as a source of lipotoxic intermediates that impair insulin signaling. Dyslipidemia has been proposed to contribute to lipid overflow and ectopic fat deposition in skeletal muscle, whereas myosteatosis-induced insulin resistance may, in turn, be linked to increased hepatic de novo lipogenesis, potentially contributing to atherogenic dyslipidemia. Epidemiological studies consistently demonstrate associations between myosteatosis and adverse lipid profiles across populations, although the magnitude and specificity of these associations vary by sex, age, ethnicity, and accompanying adipose depots such as visceral fat. Most available evidence remains cross-sectional, and standardized quantification methods are lacking. Future longitudinal and interventional studies are needed to clarify causality, define diagnostic thresholds, and determine whether improving muscle quality can mitigate cardiometabolic risk. Incorporating myosteatosis assessment into clinical practice may enhance metabolic risk stratification beyond conventional measures of muscle mass and adiposity.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"445-457"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081079","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":"Bempedoic Acid: From Guidelines to the Real World.","authors":"Jakub Michal Zimodro, Ioanna Gouni-Berthold","doi":"10.12997/jla.2026.15.3.381","DOIUrl":"10.12997/jla.2026.15.3.381","url":null,"abstract":"<p><p>Atherosclerotic cardiovascular disease remains the global leading cause of mortality. Hypercholesterolemia is a major, yet mostly insufficiently controlled, cardiovascular risk factor. Guideline-recommended lipid-lowering therapies (LLT) are underutilized, leading to low rates of low-density lipoprotein cholesterol (LDL-C) goal attainment. Poor adherence and intolerance to statins contributed to the need for developing non-statin lipid-lowering drugs. Their role increased following the concept of upfront combination LLT in patients unlikely to reach their LDL-C goal on statin monotherapy. Bempedoic acid emerged as a generally safe, efficient, and cost-effective strategy to lower LDL-C and cardiovascular risk in high- and very-high-risk individuals unable or unwilling to take statins. This updated review 1) outlines the basic pharmacology of bempedoic acid, 2) summarizes the results of clinical trials and real-world studies evaluating the efficacy and safety of bempedoic acid in the treatment of dyslipidemias, and 3) discusses the various current guidelines on the use of bempedoic acid in clinical practice.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"381-398"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081053","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":"Strenuous Exercise and Quercetin Supplementation Differentially Alter Lipid Metabolism in C57BL/6J Mice.","authors":"Halleh Shafiy, Badia Nourti, Mahdi Garelnabi","doi":"10.12997/jla.2026.15.3.519","DOIUrl":"10.12997/jla.2026.15.3.519","url":null,"abstract":"<p><strong>Objective: </strong>While moderate exercise improves lipid profiles, strenuous activity can increase oxidative stress, highlighting the potential role of antioxidants. Quercetin, a polyphenol with both antioxidant and lipid-regulating effects, may counteract exercise-induced oxidative damage and influence cholesterol metabolism. This study investigates whether combining strenuous exercise with quercetin supplementation produces distinct effects on lipoprotein remodeling, offering insights into integrative approaches for reducing cardiovascular disease risk.</p><p><strong>Methods: </strong>Forty C57BL/6 LDLr+/+ mice were randomly assigned to 4 groups (n=10): control with no exercise or quercetin (C), quercetin supplementation without exercise (Q), exercise without quercetin (E), and combined exercise with quercetin (EQ). All groups received a high-fat diet consisting of 42% fat and 1.5% cholesterol, formulated without added antioxidants. After 2 months, the mice were euthanized, and liver tissues were collected for gene expression analysis of ATP-binding cassette transporter A1 (ABCA1), proprotein convertase subtilisin/kexin type 9 (PCSK9), angiopoietin-like protein (ANGPTL) 3, ANGPTL4, peroxisome proliferator-activated receptor (PPAR) γ, apolipoprotein (APO) CIII, and APO A5 using quantitative real-time polymerase chain reaction.</p><p><strong>Results: </strong>EQ produced the most pronounced alterations in metabolic markers and lipid-regulating genes. Both Q and EQ groups showed significantly elevated total cholesterol, high-density lipoprotein, triglycerides, and glucose compared with controls, while all treated groups exhibited reduced plasma lipase levels (<i>p</i><0.05). EQ induced a significant downregulation of ABCA1 and PPARγ (<i>p</i><0.05). PCSK9 messenger RNA expression rose in Q and EQ, reaching significance only in EQ, and adiponectin levels were significantly elevated in both E and EQ (<i>p</i><0.05).</p><p><strong>Conclusion: </strong>Hepatic lipoprotein expression was modulated by the combined effects of quercetin supplementation and exercise. The observed reductions in ABCA1 and PCSK9 expressions may reflect a feedback response to enhanced clearance of circulating cholesterol.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"519-532"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081185","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 Phospholipase A₂ Superfamily in Health and Disease: From Lipid Signaling to Inflammation, Cancer, and Neurodegeneration.","authors":"Mohammad Mamun Sikder, Sanzida Akter Labony","doi":"10.12997/jla.2026.15.3.411","DOIUrl":"10.12997/jla.2026.15.3.411","url":null,"abstract":"<p><p>The phospholipase A₂ (PLA₂) superfamily comprises more than 50 enzymes that differ markedly in structure, catalytic mechanisms, and biological functions. Although all members share the ability to cleave acyl chains from membrane glycerophospholipids, many PLA₂ enzymes catalyze additional reactions that influence membrane composition, lipid signaling, and cellular homeostasis. Through these activities, PLA₂ enzymes contribute to the generation of free fatty acids, lysophospholipids, and downstream lipid mediators and participate in a wide range of physiological processes. Dysregulation of PLA₂ activity has been associated with numerous pathological conditions, including inflammation, cancer, metabolic dysfunction, neurodegeneration, and tissue injury. This review summarizes the major PLA₂ families, outlines their structural and biochemical features, and highlights emerging insights into their roles in health and disease.</p>","PeriodicalId":16284,"journal":{"name":"Journal of Lipid and Atherosclerosis","volume":"15 3","pages":"411-444"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081213","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}