Gao Zhumei, Chen Xiangmei
Department of Nephrology, The Second Hospital of Jilin University, Jilin, China.
Department of Nephrology, The First Medical Center, Chinese PLA General Hospital, Beijing, China.
Front Pharmacol. 2022 Apr 20;13:805281. doi: 10.3389/fphar.2022.805281. eCollection 2022.
The kidney is a highly metabolic organ and requires a large amount of ATP to maintain its filtration-reabsorption function, and mitochondrial fatty acid β-oxidation serves as the main source of energy to meet its functional needs. Reduced and inefficient fatty acid β-oxidation is thought to be a major mechanism contributing to kidney diseases, including acute kidney injury, chronic kidney disease and diabetic nephropathy. PPARα, AMPK, sirtuins, HIF-1, and TGF-β/SMAD3 activation have all been shown to play key roles in the regulation of fatty acid β-oxidation in kidney diseases, and restoration of fatty acid β-oxidation by modulation of these molecules can ameliorate the development of such diseases. Here, we disentangle the lipid metabolism regulation properties and potential mechanisms of mesenchymal stem cells and their extracellular vesicles, and emphasize the role of mesenchymal stem cells on lipid metabolism. This review aims to highlight the important role of fatty acid β-oxidation in the progression of kidney diseases, and to explore the fatty acid β-oxidation effects and therapeutic potential of mesenchymal stem cells for kidney diseases.
肾脏是一个高代谢器官，需要大量三磷酸腺苷（ATP）来维持其滤过-重吸收功能，而线粒体脂肪酸β-氧化是满足其功能需求的主要能量来源。脂肪酸β-氧化减少和效率低下被认为是导致肾脏疾病的主要机制，包括急性肾损伤、慢性肾脏病和糖尿病肾病。过氧化物酶体增殖物激活受体α（PPARα）、腺苷酸活化蛋白激酶（AMPK）、沉默调节蛋白、低氧诱导因子-1（HIF-1）以及转化生长因子-β/ 信号转导和转录激活因子3（TGF-β/SMAD3）的激活均已被证明在肾脏疾病中脂肪酸β-氧化的调节中起关键作用，通过调节这些分子来恢复脂肪酸β-氧化可以改善此类疾病的发展。在此，我们剖析间充质干细胞及其细胞外囊泡的脂质代谢调节特性和潜在机制，并强调间充质干细胞在脂质代谢中的作用。本综述旨在突出脂肪酸β-氧化在肾脏疾病进展中的重要作用，并探索间充质干细胞对肾脏疾病的脂肪酸β-氧化作用及治疗潜力。
