Metabolic reprogramming heterogeneity in chronic kidney disease

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.

Automated summary

Fibrosis caused by excessive accumulation of ECM is a characteristic of CKD. Myofibroblasts, responsible for ECM production, are activated by communication with injured proximal tubule and immune cells. Recent evidence shows that metabolic alterations play a significant role in renal fibrosis pathogenesis. Using omics technologies and functional data, specific metabolic shifts in different cell types have been found to play specific roles in the fibrogenic response. This review summarizes the main outcomes of metabolic reprogramming in renal fibrosis and provides a future perspective on renal fibrometabolism.