Apolipoprotein C-III (apoC-III) has emerged as a validated target for lowering triglycerides, triglyceride-rich lipoproteins, and remnant cholesterol. This review summarizes the biology of apoC-III, the genetic and clinical trial evidence supporting its inhibition, and remaining questions.

Early-onset obesity is associated with adverse cardiometabolic risk factors and early vascular changes linked to atherosclerosis, yet evidence-based treatment options for young children remain limited. The purpose of the review is to examine current evidence for lifestyle, pharmacologic, and surgical interventions for obesity management in preadolescent children, with emphasis on cardiometabolic and atherosclerotic risk.

Implementation science, a multi-method research area that integrates input from constituents and content experts, has emerged as an important tool in improving implementation of evidence-based practices. This review summarizes three ongoing implementation studies focused on identification of patients with significantly increased risk for atherosclerotic cardiovascular disease (ASCVD) due to genomic risk such as familial hypercholesterolemia (FH) within a single health system.

Lipoprotein(a) [Lp(a)], a predominantly genetically determined biomarker that remains relatively stable throughout life, is a well-established and independent risk factor for cardiovascular disease. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have demonstrated broad cardiometabolic benefits, yet their potential influence on Lp(a) remains unclear. This review synthesizes the most recent evidence at the intersection of GLP-1RAs, Lp(a), and cardiovascular disease, with particular emphasis on underlying mechanistic pathways and their potential implications for cardiovascular risk stratification and clinical outcomes.

To assess and present the current state of gene editing for reduction of atherosclerotic cardiovascular disease (ASCVD) with emphasis on technology and ongoing trials for genetic editing of protein convertase subtilisin/kexin type 9 (PCSK9).

Lipoprotein(a) [Lp(a)] is an independent, genetically determined, and causal risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis. Elevated Lp(a) affects approximately 20% of the global population and is not meaningfully modified by lifestyle intervention or existing lipid-lowering pharmacotherapy. This review summarizes the biology of Lp(a) as a therapeutic target, evaluates the efficacy of currently available lipid-lowering agents against this target, and describes the mechanistic principles, clinical evidence, and unresolved questions associated with RNA-based and emerging small-molecule and gene-editing approaches to Lp(a) reduction.

To examine the role of non-HDL cholesterol (non-HDL-C) as a predictor of coronary atherosclerosis and atherosclerotic cardiovascular disease (ASCVD) risk in South Asians, and its utility relative to LDL-C and apolipoprotein B for risk stratification and lipid-lowering therapy in this high-risk population.

Although the association of lipoprotein(a) (Lp(a)) with coronary heart disease was reported over 60 years ago, and subsequent studies have identified a causal and independent role for Lp(a) in disease, many fundamental unanswered questions persist surrounding the biology of this enigmatic lipoprotein. There remain critical questions surrounding the structure and metabolism of Lp(a) and the unique biochemical properties of Lp(a) that drive its pathogenic properties in the vasculature. These questions are critical to address as we rapidly approach the availability of drugs that can specifically lower Lp(a).

Atherosclerosis is a chronic inflammatory disease in which oxidative stress serves as a final common mechanism linking endothelial injury, lipoprotein oxidation, immune activation, and plaque progression. Since the original description of reactive oxygen species (ROS) generating and antioxidant systems in atherogenesis, substantial advances have reshaped the mechanistic and therapeutic landscape. This review provides a comprehensive update on oxidative stress in atherosclerosis, with particular emphasis on the LOX-1-NLRP3 inflammasome axis as a central driver of residual inflammatory risk.

Post-traumatic stress disorder (PTSD), a trauma- and stressor-triggered psychiatric condition affecting approximately 10 million Americans, is a major risk factor for atherosclerosis and its devastating sequelae including ischemic heart disease, stroke and hypertension. PTSD and atherosclerosis share many pathogenic mechanisms impacting the limbic system, prefrontal cortex and systemic vasculature, including hyperactivation of the sympathetic and renin-angiotensin systems, inflammation, dysregulated coagulation and altered cortisol secretion. Whether PTSD is a direct cause of atherosclerosis, or an independent co-phenomenon, is an unresolved but pivotal question.

We describe two patients with Tangier disease (TD) and provide a narrative review of its clinical features, genetics, diagnosis, and management. A literature search of PubMed and Google Scholar was performed to identify English-language publications on TD, and relevant articles were reviewed narratively.

This review assesses progress towards integrating cardiovascular disease (CVD) services within primary health care (PHC) systems in South Asia. The review examines the policy landscape, existing implementation efforts, barriers and enablers to integrated care, and the impacts of these approaches on health and health service outcomes.

This review examines how smooth muscle cell (SMC) fate transitions contribute to the central paradox of atherosclerosis: why thin-cap plaques that only mildly narrow the lumen cause most acute events, whereas many severely stenotic lesions remain stable. We propose that interactions between SMC developmental programming and local microenvironments determine whether SMCs build collagen-rich fibrous caps, undergo medial degeneration, or adopt phenotypes that weaken the vessel wall.

This paper reviews the present literature on how sex-related differences in gut dysbiosis influence vascular smooth muscle cell behavior in the pathogenesis of abdominal aortic aneurysms.

Atherosclerosis (AS), the pathological basis of atherosclerotic cardiovascular disease (ASCVD), is a chronic, progressive inflammatory disease whose major clinical events are primarily caused by plaque rupture and subsequent thrombosis. Plaque stability is critically dependent on vascular remodeling and dynamic extracellular matrix (ECM) remodeling. Accumulating evidence suggests that metabolic reprogramming is a key regulator of vascular cell phenotypic transitions and plaque progression. Among various metabolic pathways, glutamine (Gln) metabolism is of particular interest because it links nutrient availability with vascular cell function through carbon and nitrogen supply, maintenance of redox homeostasis, and generation of metabolites involved in epigenetic regulation. However, the contribution of Gln metabolism to AS progression remains incompletely understood. This review summarizes current advances in Gln metabolism and discusses its regulatory roles in vascular remodeling and plaque stability, with a focus on its implications for AS pathogenesis and therapeutic strategies.