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与艾滋病毒相关的动脉样硬化中的胆固醇外流:机制和目标
Emily Lu1, Vignesh Chidambaram2, Amudha Kumar3
1Division of Infectious Diseases, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Trends in molecular medicine
|August 30, 2025
概括
抗逆转录病毒疗法改善了艾滋病毒的治疗,但增加了动脉样硬化心血管疾病的风险. 艾滋病毒会影响胆固醇排放,这是动脉样硬化的关键过程,因此需要针对这种机制的新疗法.
科学领域:
- 生物医学
- 心血管研究
- 传染性疾病
背景情况:
- 抗逆转录病毒治疗 (ART) 使艾滋病毒感染成为一种慢性疾病.
- 携带艾滋病毒 (PLWH) 的人面临动脉样硬化心血管疾病 (ASCVD) 的风险增加.
- 高密度脂蛋白 (HDL) 的功能障碍和巨细胞的胆固醇排放有助于艾滋病毒相关的动脉样硬化.
研究的目的:
- 探索HIV引起的胆固醇排放障碍背后的分子机制.
- 审查针对PLWH中ASCVD风险的新兴疗法.
主要方法:
- 对HIV-Nef蛋白对ATP结合盒载体 (ABC) A1的影响分子机制的审查.
- 分析ART如何影响巨细胞和HDL功能.
- 探索针对逆胆固醇运输的新疗法.
主要成果:
- 通过转录后降低调节,错位化和降解,HIV Nef蛋白抑制了ABCA1介导的胆固醇外流.
- 部分恢复巨细胞和HDL功能,但观察到持续的胆固醇排放障碍.
- 新兴的疗法在增强逆胆固醇传输和减少艾滋病毒复制方面表现有前途.
结论:
- 持续的胆固醇排放障碍在PLWH治疗中有助于ASCVD风险的增加.
- 针对逆胆固醇运输和艾滋病毒复制的新型治疗方法对于管理PLWH中ASCVD至关重要.
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