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Long‐Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics‐Induced Atherosclerosis by Upregulating MARCO
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In a mouse study, polystyrene nanoplastics (50 nm) worsened atherosclerosis (hardening of the arteries) when combined with a high-fat diet. The nanoplastics accumulated in blood and artery walls, triggering immune cells to promote plaque buildup through a pathway involving long-chain acyl carnitines and the MARCO receptor. This research suggests that nanoplastic exposure could increase the risk of cardiovascular disease in people who already have risk factors like a poor diet.
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.
More Papers Like This
Long‐Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics‐Induced Atherosclerosis by Upregulating MARCO (Adv. Sci. 19/2023)
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This is a graphical abstract or cover-image entry for a research article (published in Advanced Science) that found long-chain acyl carnitines — naturally occurring metabolic molecules — make polystyrene nanoplastic-induced atherosclerosis significantly worse by activating a specific receptor (MARCO) on immune cells. The finding suggests that microplastic exposure interacts with the body's own metabolism to amplify cardiovascular disease risk.
Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
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Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
Polystyrene bead ingestion promotes atherosclerosis plaque progression via BMP signaling in mice
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Researchers found that mice fed polystyrene microplastics for 12 weeks developed worsened atherosclerosis, the buildup of fatty plaques in blood vessels. The microplastics triggered oxidative stress and activated a signaling pathway (BMP) that caused blood vessel cells to change their identity, accelerating plaque formation. The study provides evidence that microplastic ingestion could contribute to cardiovascular problems by promoting inflammation and disrupting the normal function of blood vessel walls.
Chronic Polystyrene Nanoplastics Exposure Reprograms Gene Expression, Alternative Splicing, and Disrupts Host–Microbiome–Metabolic Networks to Promote Atherosclerosis in LDLr⁻/⁻ Mice
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Tiny plastic particles (nanoplastics), similar in size to what's already been found in human arteries, made clogged-artery disease significantly worse in mice by disrupting liver function, altering gut bacteria, and throwing off protective body chemicals—all at the same time. This matters because these mice were genetically similar to how many people process cholesterol, and the same disease patterns showed up when researchers compared their data to human artery disease samples, suggesting everyday plastic exposure could be a hidden contributor to heart disease risk in people, too.
Polyethylene and Polyvinyl Chloride Nanoplastics Accelerate Atherosclerosis Through Distinct Smooth Muscle Cell Phenotypes
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Researchers found that oral exposure to polyethylene and polyvinyl chloride nanoplastics accelerated atherosclerosis in mice through distinct molecular mechanisms. Polyethylene drove smooth muscle cells toward a calcification-promoting state, while polyvinyl chloride promoted a different cell behavior linked to altered collagen metabolism, and these polymer-specific patterns were also reflected in human carotid plaque samples.
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