饮食摄入量和谷氨酸-氨酸代谢控制病理性血管硬性
Nesrine S Rachedi1, Ying Tang2, Yi-Yin Tai2
1Université Côte d'Azur, CNRS, INSERM, IPMC, IHU-RespirERA, Valbonne, France.
Cell metabolism
|May 3, 2024
概括
纤维细胞使用特定的代谢途径产生原蛋白,导致肺高血压的血管硬化. 通过饮食或药物干预来准这些途径可以减少血管硬并改善心脏功能.
科学领域:
- 心血管生物学 心血管生物学
- 代谢调节 代谢调节 代谢调节
- 纤维细胞生物学 纤维细胞生物学
背景情况:
- 被激活的纤维细胞的周血管原沉积有助于血管硬化和诸如肺高血压 (PH) 这样的疾病.
- 在血管纤维细胞中实现持续的原生物合成的代谢适应尚未得到充分理解.
研究的目的:
- 研究血管纤维细胞用于原蛋白生产的代谢途径.
- 为了确定YAP和TAZ (WWTR1) 在肺动脉附带性纤维细胞 (PAAF) 的背景下如何影响纤维细胞代谢.
主要方法:
- 研究了在炎症,缺氧和机械应激条件下PAAF中YAP和TAZ (WWTR1) 的作用.
- 分析了谷氨酸和血清蛋白与林和甘氨酸的代谢流动的关系.
- 评估了向普罗林和甘氨酸代谢对PH动物模型中的血管硬化和心血管功能的影响.
主要成果:
- 在PAAF中,炎症,缺氧和机械压力会激活YAP和TAZ.
- 激活的YAP和TAZ促进了谷氨胺和血清酶代谢,以支持用于原蛋白生产的林和甘氨酸合成.
- 在PH模型中,药物或饮食干预措施针对プロ林和甘氨酸代谢减少了血管硬化和改善了心血管功能.
结论:
- YAP和TAZ在PAAF中编排一种代谢程序,为原蛋白生物合成提供燃料.
- 向纤维细胞代谢通路为治疗血管硬化和心肺血管疾病提供了潜在的治疗策略.
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