衰老互动组:从细胞失调到与年龄有关的疾病中的治疗边界
Louay Abo Qoura1, Alexey V Churov2, Olga N Maltseva3
1Research Institute of Molecular and Cellular Medicine, Peoples' Friendship University of Russia (RUDN University), 117198, Moscow, Russia; N.N. Blokhin National Medical Research Center of Oncology (N.N. Blokhin NMRCO) of the Ministry of Health of the Russian Federation, 115478, Moscow, Russia.
Biochimica et biophysica acta. Molecular basis of disease
|September 27, 2025
概括
生物衰老涉及炎症,免疫衰老和线粒体功能障碍,导致与年龄有关的疾病. 针对这些共同的衰老机制提供了整体的健康延伸.
科学领域:
- 老年学和细胞生物学,专注于衰老的分子机制.
背景情况:
- 生物衰老的特点是细胞恒常性损失,由炎症,免疫衰老,线粒体功能障碍和基因组不稳定性驱动.
- 与衰老相关的疾病如动脉样硬化,肥胖,肉,神经退行性疾病,类风湿性关节炎和癌症都有共同的潜在衰老机制.
研究的目的:
- 审查生物衰老的相互关联机制及其在与年龄有关的疾病中的作用.
- 讨论影响衰老和疾病进展的因素,包括微生物组,性别差异和外体.
- 探索衰老生物标志物和健康延长治疗策略的进展.
主要方法:
- 关于衰老机制和相关疾病的当前知识的综合文献综述.
- 分析多omics技术和人工智能驱动的生物标志物,如表观遗传钟.
- 检查针对共享衰老路径的治疗干预措施.
主要成果:
- 确定了关键的衰老途径 (炎症,免疫衰老,线粒体功能障碍,基因组不稳定) 以及它们与多种与年龄有关的疾病的联系.
- 突出了微生物组失生症,性别差异和外体细胞沟通对衰老的影响.
- 证明了表观遗传时钟和多组学对于精确的衰老量化和风险分层的实用性.
结论:
- 衰老是一个多方面的过程,在各种疾病中都有共同的分子基础.
- 针对核心衰老机制而不是个别疾病的整体治疗干预措施有望延长健康寿命.
- 生物标志物和治疗方法的进步标志着向积极主动的,个性化的衰老干预措施的转变.
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