同型半胱氨酸
蛋白质稳态
氧化应激
高同型半胱氨酸血症
化学
肾脏疾病
硫醇
反硫化
KEAP1型
平衡
终末期肾病
生物化学
作者
Elena A. Ostrakhovitch,Siamak Tabibzadeh
出处
期刊:Advances in Clinical Chemistry
日期:2015-01-01
卷期号:: 77-106
被引量:39
标识
DOI:10.1016/bs.acc.2015.07.002
摘要
Hyperhomocysteinemia occurs in chronic- and end-stage kidney disease at the time when dialysis or transplant becomes indispensable for survival. Excessive accumulation of homocysteine (Hcy) aggravates conditions associated with imbalanced homeostasis and cellular redox thereby resulting in severe oxidative stress leading to oxidation of reduced free and protein-bound thiols. Thiol modifications such as N-homocysteinylation, sulfination, cysteinylation, glutathionylation, and sulfhydration control cellular responses that direct complex metabolic pathways. Although cysteinyl modifications are kept low, under Hcy-induced stress, thiol modifications persist thus surpassing cellular proteostasis. Here, we review mechanisms of redox regulation and show how cysteinyl modifications triggered by excess Hcy contribute development and progression of chronic kidney disease. We discuss different signaling events resulting from aberrant cysteinyl modification with a focus on transsulfuration.
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