Metabolic reprogramming heterogeneity in chronic kidney disease

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.

Keywords: fatty acid oxidation; glycolysis; kidney fibrosis; mitochondria; myofibroblasts; tubular epithelial cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Fatty Acids / metabolism
  • Fibrosis* / complications
  • Fibrosis* / metabolism
  • Fibrosis* / pathology
  • Fibrosis* / physiopathology
  • Glucose / metabolism
  • Glutamine / metabolism
  • Humans
  • Oxidative Phosphorylation
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / metabolism
  • Renal Insufficiency, Chronic* / pathology
  • Renal Insufficiency, Chronic* / physiopathology


  • Glucose
  • Glutamine
  • Fatty Acids