Metabolomics Assessment of Volume Overload-Induced Heart Failure and Oxidative Stress in the Kidney

被引:4
作者
Tang, Hsiang-Yu [1 ]
Huang, Jyh-En [2 ]
Tsau, Ming-Tong [1 ]
Chang, Chi-Jen [3 ,4 ]
Tung, Ying-Chang [3 ,4 ]
Lin, Gigin [5 ,6 ,7 ,8 ]
Cheng, Mei-Ling [1 ,2 ,5 ,9 ]
机构
[1] Chang Gung Univ, Hlth Aging Res Ctr, Metabol Core Lab, Taoyuan 33302, Taiwan
[2] Chang Gung Univ, Grad Inst Biomed Sci, Coll Med, Taoyuan 33302, Taiwan
[3] Linkou Chang Gung Mem Hosp, Dept Cardiol, Taoyuan 33323, Taiwan
[4] Chang Gung Univ, Coll Med, Sch Med, Taoyuan 33302, Taiwan
[5] Chang Gung Mem Hosp, Clin Metabol Core Lab, Taoyuan 33323, Taiwan
[6] Chang Gung Mem Hosp Linkou, Dept Med Imaging & Intervent, Taoyuan 33323, Taiwan
[7] Chang Gung Univ, Inst Radiol Res, Imaging Core Lab, Taoyuan 33323, Taiwan
[8] Chang Gung Univ, Dept Med Imaging & Radiol Sci, Taoyuan 33302, Taiwan
[9] Chang Gung Univ, Coll Med, Dept Biomed Sci, Taoyuan 33302, Taiwan
关键词
heart failure; volume overload; aortocaval fistula; cardiorenal syndrome; kidney; oxidative stress; uric acid; taurine; URIC-ACID; CARDIORENAL SYNDROME; TAURINE; METABOLISM; PROTECTS; OUTCOMES; PLASMA; ANEMIA; TARGET; TISSUE;
D O I
10.3390/metabo13111165
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The incidence of heart failure (HF) is increasing and is associated with a poor prognosis. Moreover, HF often coexists with renal dysfunction and is associated with a worsened outcome. In many experimental studies on cardiac dysfunction, the function of other organs was either not addressed or did not show any decline. Until now, the exact mechanisms for initiating and sustaining this interaction are still unknown. The objective of this study is to use volume overload to induce cardiac hypertrophy and HF in aortocaval fistula (ACF) rat models, and to elucidate how volume overload affects metabolic changes in the kidney, even with normal renal function, in HF. The results showed the metabolic changes between control and ACF rats, including taurine metabolism; purine metabolism; glycine, serine, and threonine metabolism; glycerophospholipid metabolism; and histidine metabolism. Increasing the downstream purine metabolism from inosine to uric acid in the kidneys of ACF rats induced oxidative stress through xanthine oxidase. This result was consistent with HK-2 cells treated with xanthine and xanthine oxidase. Under oxidative stress, taurine accumulation was observed in ACF rats, indicating increased activity of the hypotaurine-taurine pathway as a defense mechanism against oxidative stress in the kidney. Another antioxidant, ascorbic acid 2-sulfate, showed lower levels in ACF rats, indicating that the kidneys experience elevated oxidative stress due to volume overload and HF. In summary, metabolic profiles are more sensitive than clinical parameters in reacting to damage to the kidney in HF.
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页数:14
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