甲基胺和三甲基胺N-氧化物:两个尿素作用者,不同的作用
Sam Hobson1, Abdul Rashid Qureshi1, Jonaz Ripswedan2,3
1Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
European journal of clinical investigation
|August 7, 2023
概括
三甲基胺N-氧化物 (TMAO) 在慢性病 (CKD) 患者中促进血管化,与甲基胺 (PAG) 不同. 这两种毒素都诱导氧化应激,突出TMAO作为潜在的治疗点,以减少CKD中的心血管风险.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 心血管医学 心血管医学
- 生物化学 生物化学
背景情况:
- 慢性病 (CKD) 患者面临心血管 (CV) 风险升高,部分原因是中枢血管化.
- 像三甲基胺N氧化物 (TMAO) 这样的肠道衍生尿性毒素与酸沉积有关.
- 在CKD血管化中,乙谷氨 (PAG) 的促化潜力仍未得到充分研究.
研究的目的:
- 研究TMAO和PAG对脏衰竭患者血管化的影响.
- 为了将尿液中毒素度与冠状动脉化 (CAC) 和腹膜动脉化得分相关联.
- 为了确定TMAO和PAG在血管光滑肌细胞和相关途径上的体外化作用.
主要方法:
- 在120名接受活体捐献者移植 (LD-KTx) 的功能衰竭患者中进行了观察性,横截面研究.
- 测量尿液中毒素度 (TMAO,PAG) 和它们与血管化评分 (CAC,胃上动脉) 的相关性.
- 用TMAO或PAG进行血管光滑肌细胞的体外化,以评估化和氧化应激.
主要成果:
- 在功能衰竭患者中,TMAO,但不是PAG,显示出与CAC得分的独立关联.
- 两种毒素都与上胃动脉化无关;然而,PAG与8-氧化瓜诺辛相关.
- 在体外,TMAO促进了酸沉积,这两种毒素都诱导了氧化应激.
结论:
- 翻译数据证实了TMAO在CKD中的促化作用.
- TMAO和PAG都诱导自由基的产生,导致血管损伤.
- 向TMAO可能是一种治疗策略,以减轻CKD患者的心血管死亡率.
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