AIM To investigate the molecular, structural, and functional impact of aerosols from candidate modified risk tobacco products (cMRTP), the Carbon Heated Tobacco Product (CHTP) 1.2 and Tobacco Heating System (THS) 2.2, compared with that of mainstream cigarette smoke (CS) on the cardiovascular system of ApoE-/- mice. METHODS Female ApoE-/- mice were exposed to aerosols from THS 2.2 and CHTP 1.2 or to CS from the 3R4F reference cigarette for up to 6 months at matching nicotine concentrations. A Cessation and a Switching group (3 months exposure to 3R4F CS followed by filtered air or CHTP 1.2 for 3 months) were included. Cardiovascular effects were investigated by echocardiographic, histopathological, immunohistochemical, and transcriptomics analyses. RESULTS Continuous exposure to cMRTP aerosols did not affect atherosclerosis progression, heart function, left ventricular (LV) structure, or the cardiovascular transcriptome. Exposure to 3R4F CS triggered atherosclerosis progression, reduced systolic ejection fraction and fractional shortening, caused heart LV hypertrophy, and initiated significant dysregulation in the transcriptomes of the heart ventricle and thoracic aorta. Importantly, the structural, functional, and molecular changes caused by 3R4F CS were improved in the smoking cessation and switching groups. CONCLUSION Exposure to cMRTP aerosols lacked most of the CS exposure-related functional, structural, and molecular effects. Smoking cessation or switching to CHTP 1.2 aerosol caused similar recovery from the 3R4F CS effects in the ApoE-/- model, with no further acceleration of plaque progression beyond the aging-related rate.

中文翻译：

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与香烟烟雾相比，暴露于候选改良风险烟草产品、碳加热烟草产品 1.2 和烟草加热系统 2.2 气溶胶的 ApoE-/- 小鼠对心血管系统的结构、功能和分子影响。


目的 与主流卷烟烟雾 (CS) 相比，研究候选改良风险烟草产品 (cMRTP)、碳加热烟草产品 (CHTP) 1.2 和烟草加热系统 (THS) 2.2 的气溶胶对分子、结构和功能的影响）对 ApoE-/- 小鼠心血管系统的影响。方法 雌性 ApoE-/- 小鼠在匹配的尼古丁浓度下暴露于 THS 2.2 和 CHTP 1.2 的气溶胶或 3R4F 参考香烟的 CS 长达 6 个月。包括戒烟组和转换组（接触 3R4F CS 3 个月，然后接触过滤空气或 CHTP 1.2 3 个月）。通过超声心动图、组织病理学、免疫组织化学和转录组学分析来研究心血管效应。结果 持续暴露于 cMRTP 气雾剂不会影响动脉粥样硬化进展、心脏功能、左心室 (LV) 结构或心血管转录组。暴露于 3R4F CS 会引发动脉粥样硬化进展，收缩期射血分数和缩短分数降低，导致心脏左室肥厚，并引发心室和胸主动脉转录组的显着失调。重要的是，戒烟组和转换组中 3R4F CS 引起的结构、功能和分子变化均得到改善。结论 暴露于 cMRTP 气溶胶缺乏大多数与 CS 暴露相关的功能、结构和分子效应。戒烟或改用 CHTP 1.2 气雾剂导致 ApoE-/- 模型中 3R4F CS 效应的类似恢复，并且斑块进展没有进一步加速超过衰老相关速率。