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衰老的巨细胞通过增加抗血管原体VEGF-A165B表达来促进与年龄相关的再血管化障碍
Minghong Chen1,2,3, Junyu Chen1,2,3, Yu Liu3,4
1Department of Geriatric Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Aging cell
|April 17, 2025
概括
老化中的衰老巨细胞通过促进炎症和内皮功能障碍,阻碍肢体缺血后的血管修复. 针对这些衰老细胞可能会改善周围动脉疾病的老年患者的血管再生.
科学领域:
- 血管生物学 血管生物学
- 衰老研究研究 衰老研究
- 免疫学 免疫学 免疫学
背景情况:
- 周围动脉疾病 (PAD) 在老年人中很普遍,在临床再血管化试验中取得的成功有限.
- 衰老会影响免疫细胞,可能会损害血管再生,但老化巨细胞在缺血组织中的作用尚不清楚.
研究的目的:
- 研究老老鼠缺血后肢肌中的巨细胞的特征和功能.
- 确定衰老的巨细胞对血管再生的影响,并确定潜在的机制.
主要方法:
- 对老鼠缺血后肢肌肉中巨细胞的分析.
- 在患有后肢缺血症的小鼠身上进行巨细胞移植实验.
- 评估内皮功能和血管内皮生长因子A-165B (VEGF-A165B) 的水平.
- 与患者数据的相关性分析 (PAD患者,脚-手臂指数).
主要成果:
- 老年小鼠缺血肌中的巨细胞表现出衰老和一种炎症性表型.
- 在小鼠模型中,移植的衰老性巨细胞显著抑制了重血管化.
- 衰老的巨细胞通过增加VEGF-A165B的表达和分泌来损害内皮功能.
- 在老年PAD患者中观察到血VEGF-A165B水平升高和脚下腕指数 (ABI).
结论:
- 衰老的巨细胞有助于衰老中的血管再生受损.
- 由衰老的巨细胞介导的VEGF-A165B是内皮功能障碍和减少复血管化的关键因素.
- 针对衰老的巨细胞为PAD中与年龄相关的血管并发症提供了潜在的治疗策略.
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