Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Visceral adipose tissue (VAT)-derived extracellular vesicles (EVs) have emerged as key mediators of inter-organ communication, yet their role in nicotine-induced atherosclerosis remains poorly defined. Here, we demonstrate that nicotine markedly enhances secretion of VAT-EVs and that these EVs are preferentially internalized by macrophages within atherosclerotic plaques, thereby accelerating lesion progression. Functionally, nicotine-induced VAT-EVs promote macrophage inflammation, oxidative stress, and foam cell formation. High-throughput profiling identified miR-210-3p as a dominant pro-atherogenic cargo within VAT-EVs, and its inhibition significantly attenuated nicotine-induced atherosclerosis in vivo . Mechanistically, miR-210-3p directly targets Krüppel-like factor 7 (KLF7), amplifying macrophage inflammatory responses and promoting plaque progression. Collectively, these findings uncover a previously unrecognized role of adipose-derived EVs in smoking-related vascular injury and highlight EV-derived miR-210-3p as a promising therapeutic target in nicotine-associated atherosclerosis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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