慢性病中的酸盐毒性和血管化:使用传输电子显微镜更仔细地观察
Ying Yang1,2, Ke Yang2,3, Yuxin Xiong1,2
1Department of Endocrinology, the Affiliated Hospital of Yunnan University and the Second People's Hospital of Yunnan Province, Kunming, Yunnan, 650021, China.
Current protein & peptide science
|July 27, 2023
概括
慢性病 (CKD) 和末期病 (ESRD) 中的高酸血与严重并发症有关. 本综述探讨了酸盐毒性,FGF-23/Klotho轴,以及CKD中的血管化.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 心血管科学 心血管科学
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 过血是慢性病 (CKD) 和末期病 (ESRD) 的重要并发症,独立与血管化,心血管疾病,骨矿物质疾病和死亡率有关.
- 纤维细胞生长因子-23 (FGF-23) /Klotho轴对酸盐稳定至关重要,脏Klotho产量减少导致CKD中酸盐水平升高.
- 相关的并发症包括石灰症,管间疾病,骨质疏松症和尿路性心肌病.
研究的目的:
- 审查酸盐平衡和毒性在CKD和ESRD中的多方面的作用.
- 检查FGF-23/Klotho轴对高酸血症及其后果的贡献.
- 探索胸前大动脉的超结构重塑及其与血管化的关系,并结合动物模型的见解.
主要方法:
- 对CKD/ESRD中高酸血症,FGF-23,Klotho和血管化现有文献的综述.
- 纳入胸前大动脉的超结构重塑数据.
- 利用来自9周大雄异合体 (mRen2) 27 (Ren2) 鼠标模型和Zucker肥胖 (fa/fa) 鼠标模型的数据.
主要成果:
- 高酸血是血管化,心血管疾病和CKD/ESRD死亡率的关键驱动因素.
- FGF-23/Klotho轴的失调有助于酸盐的保留和相关的病理.
- 动物模型展示了与血管化有关的大动脉重塑,并提供了对石形成的见解.
结论:
- 酸盐稳态,毒性和FGF-23/Klotho轴对于理解CKD/ESRD进展和并发症至关重要.
- 由高酸血症驱动的血管化涉及复杂的细胞和分子机制,包括氧化应激和炎症.
- 对这些途径的进一步研究对于开发针对CKD/ESRD患者的向疗法至关重要.
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