Institute of Experimental Medicine and Systems Biology, RWTH Aachen University Hospital, Aachen, Germany.
FEBS Open Bio. 2023 Jul;13(7):1154-1163. doi: 10.1002/2211-5463.13568. Epub 2023 Feb 14.
Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alterations in metabolism are not only a feature of but also play an influential role in the pathogenesis of renal fibrosis. The application of omics technologies to cell-tracing animal models and follow-up functional data suggest that cell-type-specific metabolic shifts have particular roles in the fibrogenic response. In this review, we cover the main metabolic reprogramming outcomes in renal fibrosis and provide a future perspective on the field of renal fibrometabolism.
细胞外基质（ECM）过度积累导致的纤维化是慢性肾脏病（CKD）的标志。肌成纤维细胞是 ECM 产生的细胞，它们通过与受损的近端肾小管和免疫细胞的相互作用而被激活。新出现的证据表明，代谢改变不仅是肾脏纤维化发病机制的一个特征，而且还起着重要作用。组学技术在细胞示踪动物模型和后续功能数据中的应用表明，细胞类型特异性的代谢变化在纤维生成反应中具有特殊作用。在这篇综述中，我们涵盖了肾脏纤维化中主要的代谢重编程结果，并对肾脏纤维代谢领域的未来前景进行了展望。
