Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury

被引:3
|
作者
Zhao, Limei [1 ]
Hao, Yajie [1 ]
Tang, Shuqin [1 ]
Han, Xiutao [2 ]
Li, Rongshan [3 ]
Zhou, Xiaoshuang [3 ]
机构
[1] Shanxi Med Univ, Clin Med Coll 5, Taiyuan, Shanxi, Peoples R China
[2] Shanxi Univ Chinese Med, Clin Coll 3, Jinzhong, Shanxi, Peoples R China
[3] Shanxi Med Univ, Shanxi Prov Peoples Hosp, Clin Med Coll 5, Dept Nephrol, Taiyuan, Shanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
acute kidney injury; renal tubular epithelial cells; energy metabolism; programmed cell death; therapeutic; ISCHEMIA-REPERFUSION INJURY; AMINO-ACID; MITOCHONDRIAL-FUNCTION; BETA-OXIDATION; GLUCOSE; PROTEIN; ACTIVATION; 20-HETE; GLUTAMINE; AUTOPHAGY;
D O I
10.3389/fcell.2023.1276217
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Acute kidney injury (AKI) induces significant energy metabolic reprogramming in renal tubular epithelial cells (TECs), thereby altering lipid, glucose, and amino acid metabolism. The changes in lipid metabolism encompass not only the downregulation of fatty acid oxidation (FAO) but also changes in cell membrane lipids and triglycerides metabolism. Regarding glucose metabolism, AKI leads to increased glycolysis, activation of the pentose phosphate pathway (PPP), inhibition of gluconeogenesis, and upregulation of the polyol pathway. Research indicates that inhibiting glycolysis, promoting the PPP, and blocking the polyol pathway exhibit a protective effect on AKI-affected kidneys. Additionally, changes in amino acid metabolism, including branched-chain amino acids, glutamine, arginine, and tryptophan, play an important role in AKI progression. These metabolic changes are closely related to the programmed cell death of renal TECs, involving autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis. Notably, abnormal intracellular lipid accumulation can impede autophagic clearance, further exacerbating lipid accumulation and compromising autophagic function, forming a vicious cycle. Recent studies have demonstrated the potential of ameliorating AKI-induced kidney damage through calorie and dietary restriction. Consequently, modifying the energy metabolism of renal TECs and dietary patterns may be an effective strategy for AKI treatment.
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页数:19
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