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在癌症幸存者的动脉样硬化发展的潜在分子机制
Priyanka Banerjee1, Julia Enterría Rosales2,3, Khanh Chau1
1Center for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX, United States.
Frontiers in cardiovascular medicine
|June 19, 2023
概括
癌症治疗可以导致内皮细胞发展与衰老相关的干细胞 (SAS),增加幸存者的心血管疾病 (CVD) 风险. 准这些SAS细胞为预防心血管疾病提供了潜在的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 癌症生物学 癌症生物学
- 细胞衰老 细胞衰老
背景情况:
- 癌症幸存者面临着动脉样硬化心血管疾病 (CVD) 的高风险.
- 在幸存者中,将癌症治疗与心血管疾病联系在一起的机制尚未完全理解.
- 化疗可以诱导衰老细胞 (SAS) 中的干性表型.
研究的目的:
- 阐明衰老相关干细胞 (SAS) 诱导在内皮细胞 (ECs) 的机制.
- 了解SAS-ECs对癌症幸存者的动脉样硬化的贡献.
- 探索在这个人群中管理心血管疾病的潜在治疗点.
主要方法:
- 关于EC衰老,SAS和动脉样硬化的当前文献的综述.
- 分析了受干扰流和电离辐射引起的EC衰老所涉及的途径.
- 探索信号通路,例如p90RSK/TERF2IP,TGFβR1/SMAD,以及BH4.4等信号通路.
主要成果:
- 癌症治疗可以诱导EC衰老,促进SAS表型.
- SAS-ECs有助于癌症幸存者的动脉样硬化发展.
- 特定的信号通路与SAS诱导和EC衰老有关.
结论:
- 针对SAS表型的老化EC是癌症幸存者的心血管疾病的有前途的治疗策略.
- 了解衰老途径可以为心血管健康带来新的干预措施.
- 区分衰老类型和途径对于有效的治疗开发至关重要.
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