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Purpose of Review: Low-density lipoprotein (LDL) poses a risk for atherosclerotic cardiovascular disease (ASCVD). As LDL comprises various subtypes differing in charge, density, and size, understanding their specific impact on ASCVD is crucial. Two highly atherogenic LDL subtypes—electronegative LDL (L5) and Lp(a)—induce vascular cell apoptosis and atherosclerotic changes independent of plasma cholesterol levels, and their mechanisms warrant further investigation. Here, we have compared the roles of L5 and Lp(a) in the development of ASCVD. Recent Findings: Lp(a) tends to accumulate in artery walls, promoting plaque formation and potentially triggering atherosclerosis progression through prothrombotic or antifibrinolytic effects. High Lp(a) levels correlate with calcific aortic stenosis and atherothrombosis risk. L5 can induce endothelial cell apoptosis and increase vascular permeability, inflammation, and atherogenesis, playing a key role in initiating atherosclerosis. Elevated L5 levels in certain high-risk populations may serve as a distinctive predictor of ASCVD. Summary: L5 and Lp(a) are both atherogenic lipoproteins contributing to ASCVD through distinct mechanisms. Lp(a) has garnered attention, but equal consideration should be given to L5. [ABSTRACT FROM AUTHOR]

Purpose of Review: In this review, we explore the intriguing and evolving connections between bacterial extracellular membrane nanovesicles (BEMNs) and atherosclerosis development, highlighting the evidence on molecular mechanisms by which BEMNs can promote the athero-inflammatory process that is central to the progression of atherosclerosis. Recent Findings: Atherosclerosis is a chronic inflammatory disease primarily driven by metabolic and lifestyle factors; however, some studies have suggested that bacterial infections may contribute to the development of both atherogenesis and inflammation in atherosclerotic lesions. In particular, the participation of BEMNs in atherosclerosis pathogenesis has attracted special attention. Summary: We provide some general insights into how the immune system responds to potential threats such as BEMNs during the development of atherosclerosis. A comprehensive understanding of contribution of BEMNs to atherosclerosis pathogenesis may lead to the development of targeted interventions for the prevention and treatment of the disease. [ABSTRACT FROM AUTHOR]

Electronegative low-density lipoprotein (LDL) found in human plasma is highly atherogenic, and its level is elevated in individuals with increased cardiovascular risk. In this review, we summarize the available data regarding the elevation of the levels of electronegative LDL in the plasma of patients with various diseases. In addition, we discuss the harmful effects and underlying mechanisms of electronegative LDL in various cell types. We also highlight the known biochemical properties of electronegative LDL that may contribute to its atherogenic functions, including its lipid and protein composition, enzymatic activities, and structural features. Given the increasing recognition of electronegative LDL as a potential biomarker and therapeutic target for the prevention of cardiovascular disease, key future goals include the development of a standard method for the detection of electronegative LDL that can be used in a large-scale population survey and the identification and testing of strategies for eliminating electronegative LDL from the blood. [ABSTRACT FROM AUTHOR]

Myeloperoxidase (MPO), a member of the heme peroxidase superfamily, is a leukocyte-derived enzyme that generates reactive intermediates, leading to oxidative damage of host lipids and proteins. It has been shown that MPO is present within atherosclerotic plaque in human arteries and contributes to atherogenesis by catalyzing oxidative reactions in the vascular wall. This review provides an overview of the analytical and pathophysiologic characteristics of MPO and summarizes the possible clinical applicability of MPO as a marker for diagnosis of acute coronary syndrome and a marker for prediction of cardiovascular disease. [ABSTRACT FROM AUTHOR]