Long‐Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics‐Induced Atherosclerosis by Upregulating MARCO

Abstract

Exposure to micro‐ and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but the underlying mechanism remains unclear. To address this bottleneck, ApoE−/− mice are exposed to 2.5–250 mg kg−1 polystyrene nanoplastics (PS‐NPs, 50 nm) by oral gavage with a high‐fat diet for 19 weeks. It is found that PS‐NPs in blood and aorta of mouse exacerbate the artery stiffness and promote atherosclerotic plaque formation. PS‐NPs activate phagocytosis of M1‐macrophage in the aorta, manifesting as upregulation of macrophage receptor with collagenous structure (MARCO). Moreover, PS‐NPs disrupt lipid metabolism and increase long‐chain acyl carnitines (LCACs). LCAC accumulation is attributed to the PS‐NP‐inhibited hepatic carnitine palmitoyltransferase 2. PS‐NPs, as well as LCACs alone, aggravate lipid accumulation via upregulating MARCO in the oxidized low‐density lipoprotein‐activated foam cells. Finally, synergistic effects of PS‐NPs and LCACs on increasing total cholesterol in foam cells are found. Overall, this study indicates that LCACs aggravate PS‐NP‐induced atherosclerosis by upregulating MARCO. This study offers new insight into the mechanisms underlying MNP‐induced cardiovascular toxicity, and highlights the combined effects of MNPs with endogenous metabolites on the cardiovascular system, which warrant further study.

Unraveling Intracellular Protein Corona Components of Nanoplastics via Photocatalytic Protein Proximity Labeling

“…The Shuler group systematically investigated how cellular metabolic homeostasis was interfered with by nanoplastic particles in cells . Huang and Jin groups discovered that exposure of polystyrene (PS) nanoplastic particles in the liver and cardiovascular system deteriorated cellular lipid metabolism by reducing digestion. , Our group recently revealed that nanoplastics can stress liver cells via destabilizing the cellular proteome and disturbing the protein homeostasis network . However, these above-mentioned works reveal limited information regarding the composition of the protein corona for nanoplastics.…”

Reactive Oxygen Species-Responsive Sequentially Targeted AIE Fluorescent Probe for Precisely Identifying the Atherosclerotic Plaques

“…4,5 Meanwhile, macrophages play a critical role in uptaking the oxidized low density lipoprotein (ox-LDL) to deteriorate into the foam cells, simultaneously releasing various inflammatory factors and then inducing the formation of atherosclerotic plaque. 6,7 Clinical study has found that the foam cell-rich atherosclerotic plaque is prone to rupture into thrombus, inducing some fatal complications such as myocardial infarction and stroke. 8,9 Thence, it is highly important to efficiently recognize the foam cells and then precisely identify the morphology and disperse distribution of the plaques for physicians to make timely clinical decisions and perform proactive interventions as early as possible.…”

“…Cardiovascular diseases (CVDs) are the leading cause of global mortality and disability, accounting for almost half of total death annually. − Atherosclerosis (AS) is an inflammation-driven chronic disease caused by the asymptomatic buildup of plaques on the arterial wall to the formation of atherosclerotic plaque, even the rupture of plaque. , Meanwhile, macrophages play a critical role in uptaking the oxidized low density lipoprotein (ox-LDL) to deteriorate into the foam cells, simultaneously releasing various inflammatory factors and then inducing the formation of atherosclerotic plaque. , Clinical study has found that the foam cell-rich atherosclerotic plaque is prone to rupture into thrombus, inducing some fatal complications such as myocardial infarction and stroke. , Thence, it is highly important to efficiently recognize the foam cells and then precisely identify the morphology and disperse distribution of the plaques for physicians to make timely clinical decisions and perform proactive interventions as early as possible …”

Surface-Charge-Driven Ferroptosis and Mitochondrial Dysfunction Is Involved in Toxicity Diversity in the Marine Bivalve Exposed to Nanoplastics

“…In recent decades, oceans have faced escalating pollution, notably a substantial surge in plastic waste, now accounting for approximately 85% of marine litter. − This pervasive issue continues as plastics break down into microplastics (MPs, <5 mm) and further degrade into more hazardous nanoplastics (NPs, <1 μm) with varying surface properties (e.g., charge). − Comprehensive research has underscored the detrimental effects of NP overexposure on various aquatic invertebrates. , These NPs, when ingested, tend to accumulate within critical organs such as gills and digestive glands, , and may subsequently migrate to peripheral tissues and the circulatory system, leading to widespread toxicity. , For example, an investigation reported genotoxicity and damage to the intestinal mucosal barrier in Corbicula fluminea after a 10-day exposure to polystyrene (PS) NPs (3.5 × 10 8 –3.5 × 10 9 particles/mL), suggesting the potential apoptosis induction . Despite these illuminating insights, studies have mainly focused on biochemical and molecular alterations .…”

“…1,7 These NPs, when ingested, tend to accumulate within critical organs such as gills and digestive glands, 7,8 and may subsequently migrate to peripheral tissues and the circulatory system, leading to widespread toxicity. 9,10 For example, an investigation reported genotoxicity and damage to the intestinal mucosal barrier in Corbicula fluminea after a 10-day exposure to polystyrene (PS) NPs (3.5 × 10 8 −3.5 × 10 9 particles/mL), suggesting the potential apoptosis induction. 7 Despite these illuminating insights, studies have mainly focused on biochemical and molecular alterations.…”