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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.
Microplastics and Nanoplastics Qin Qiong is revered as a venerable guardian deity in ancient Chinese mythology. Similarly, macrophages serve as its protectors within the cardiovascular system. In article number 2205876, Yizhou Zhong, Zhenlie Huang, and co‐workers unveil that when the cardiovascular system is exposed to micro‐ and nanoplastics (MNPs), macrophages face not only the direct assault from the MNPs but also simultaneous aggression from long‐chain acylcarnitines, a kind of endogenous chemical compound. These findings have the potential to aid in managing the escalating health risks imposed on humanity by increasing MNP exposure. [Image: see text]
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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.
Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation
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Researchers used network toxicology analysis and laboratory experiments to investigate how polyethylene terephthalate microplastics may contribute to atherosclerosis. They identified several molecular targets and biological pathways through which these microplastics could promote plaque formation in blood vessels. The study provides preliminary evidence that a commonly encountered type of microplastic may interact with cardiovascular disease mechanisms, though further research is needed to confirm these findings.
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Researchers used network toxicology and gene analysis to investigate how PET microplastics may influence atherosclerosis, the buildup of plaque in arteries. They identified specific genes involved in inflammation and immune cell signaling that are affected by both PET exposure and atherosclerosis development. The study suggests that microplastic exposure could worsen cardiovascular disease through shared inflammatory pathways.
Microplastics. a New Risk Factor for Atherosclerotic Cardiovascular Disease
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This paper reviews emerging evidence linking microplastic exposure to atherosclerotic cardiovascular disease, noting that MPs have been detected in arterial plaques and human tissues and may contribute to cardiovascular risk through inflammation, oxidative stress, and endothelial disruption.
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Researchers reviewed growing clinical and experimental evidence that micro- and nanoplastics can act as non-conventional cardiovascular risk factors, with MNPs detected directly within atherosclerotic plaques where their presence correlates with enhanced inflammatory activity, plaque instability, and worse cardiovascular outcomes—suggesting MNPs amplify established cardiometabolic risks through oxidative stress and endothelial dysfunction.
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