Farra Yasmeen M, Sabnis Simone, Matz Jacqueline, Wilker Hannah, Williams Victoria A, Trejo Oliver, Kim Hannah, Rivera Cristobal, Vlahos John, Ramkhelawon Bhama, Oakes Jessica M, Bellini Chiara
Department of Bioengineering, Northeastern University, Boston, MA (Y.M.F., S.S., J.M., H.W., V.A.W., O.T., H.K., J.M.O., C.B.).
Division of Vascular and Endovascular Surgery, Department of Surgery, New York University Langone Medical Center. (C.R., J.V., B.R.).
Arterioscler Thromb Vasc Biol. 2025 Jul 24. doi: 10.1161/ATVBAHA.125.320908.
Electronic cigarettes (e-cigarettes) are the most used tobacco product among youth, and adults who smoke combustible cigarettes favor e-cigarettes over approved cessation aids. Despite the lower perceived harm of vaping compared with smoking, acute inhalation of e-cigarette aerosol elicits cardiovascular responses that may lead to persistent damage when repeated over time.
We exposed female hypercholesterolemic mice to either pod-mod e-cigarette aerosol or filtered air daily for 24 weeks. We assessed the long-term effects of vaping on aortic stiffness and vasoreactivity while investigating the underlying cellular and molecular mechanisms of injury.
Chronic inhalation of e-cigarette aerosol triggered the accumulation of inflammatory signals systemically and within aortic tissues, as well as T-lymphocyte accrual in the aortic wall. Limited eNOS (endothelial nitric oxide synthase) expression and enhanced superoxide radical production curbed NO bioavailability in the aorta of mice exposed to e-cigarette aerosol despite iNOS (inducible nitric oxide synthase) induction, impairing the endothelium-dependent vasodilation that regulates blood flow distribution. Inhalation of e-cigarette aerosol thickened and stiffened aortic tissues via collagen deposition and remodeling, hindering the storage of elastic energy and limiting the cyclic distensibility that enables the aorta to function as a pressure reservoir. These effects combined contributed to raising systolic and pulse pressure above control levels.
Chronic inhalation of aerosol from pod-mod e-cigarettes promotes oxidative stress, inflammation, and fibrosis within aortic tissues, significantly impairing passive and vasoactive aortic functions. This evidence provides new insights into the biological processes that increase the risk of adverse cardiovascular events as a result of pod-mod e-cigarette vaping.
电子烟是青少年中使用最广泛的烟草制品,而吸传统可燃香烟的成年人更青睐电子烟而非获批的戒烟辅助工具。尽管与吸烟相比,人们认为吸电子烟的危害较小,但急性吸入电子烟烟雾会引发心血管反应,若长期反复吸入,可能会导致持续性损害。
我们将雌性高胆固醇血症小鼠每天暴露于盒式电子烟烟雾或过滤空气中,持续24周。我们评估了吸电子烟对主动脉僵硬度和血管反应性的长期影响,同时研究损伤的潜在细胞和分子机制。
长期吸入电子烟烟雾会引发全身及主动脉组织内炎症信号的积累,以及主动脉壁中T淋巴细胞的积聚。尽管诱导了诱导型一氧化氮合酶(iNOS),但暴露于电子烟烟雾的小鼠主动脉中内皮型一氧化氮合酶(eNOS)表达受限,超氧自由基生成增加,抑制了一氧化氮(NO)的生物利用度,损害了调节血流分布的内皮依赖性血管舒张功能。吸入电子烟烟雾通过胶原蛋白沉积和重塑使主动脉组织增厚、变硬,阻碍了弹性能量的储存,并限制了使主动脉作为压力储存器发挥作用的周期性扩张能力。这些影响共同导致收缩压和脉压升高至对照水平以上。
长期吸入盒式电子烟烟雾会促进主动脉组织内的氧化应激、炎症和纤维化,显著损害主动脉的被动和血管活性功能。这一证据为因吸盒式电子烟而增加不良心血管事件风险的生物学过程提供了新的见解。