چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Acute kidney injury (AKI), a rapid drop in kidney function, displays high mortality and morbidity, and its repeated or severe status can shift into chronic kidney disease (CKD) or even end-stage renal disease (ESRD). How and which events cause AKI still is controversial. In addition, no specific therapies have emerged that can attenuate AKI or expedite recovery. Some central mechanisms including tubular epithelial cells (TECs) injury, endothelial injury, renal cell apoptosis, and necrosis signaling cascades, and inflammation have been reported in the pathophysiology of AKI. However, the timing of the activation of each pathway, their interactions, and the hierarchy of these pathways remain unknown. The main molecular mechanisms that might be complicated in this process are the mitochondrial impairment and alteration/shifting of cellular metabolites (e.g., acetyl-CoA and NAD+/NADH) acting as cofactors to alter the activities of many enzymes, for instance, Sirtuins. Moreover, alteration of mitochondrial structure over the fusion and fission mechanisms can regulate cellular signaling pathways by modifying the rate of ROS generation and metabolic activities. The aim of this review is to better understand the underlying pathophysiological and molecular mechanisms of AKI. Additionally, we predicted the main other molecular players in interaction with Sirtuins as energy/stresses monitoring proteins for the development of future approaches in the treatment or prevention of ischemic AKI. |
| نویسنده | نفر چندم مقاله |
|---|---|
| یلدا رهبرسعادت | اول |
| سید مهدی حسینی یان خطیبی | دوم |
| محمد رضا اردلان | سوم |
| ابوالفضل برزگری | چهارم |
| سپیده زنونی واحد | پنجم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| Molecular pathophysiology of acute kidney injury.pdf | 1399/07/10 | 2871259 | دانلود |
