Renal fibrosis is a common pathway toward chronic kidney disease (CKD) and is the main pathological predecessor for end-stage renal disease; thus, preventing progressive CKD and renal fibrosis is essential to reducing their consequential morbidity and mortality. Emerging evidence has connected renal fibrosis to metabolic reprogramming; abnormalities in energy metabolism pathways, such as glycolysis, the tricarboxylic acid cycle, and lipid metabolism, are known to cause diseases of diverse etiologies. Cytokine interventions in affected metabolic pathways may significantly reduce the degree of fibrosis, highlighting therapeutic targets for drug development for renal fibrosis. Here, we discuss the relationship between glycolysis, lipid metabolism, mitochondrial and peroxisome dysfunction, and renal fibrosis in detail and propose that targeted therapies for specific metabolic pathways are expected to represent the next generation of treatments for renal fibrosis.
Keywords: Fatty acid oxidation; Glycolysis; Mitochondrial dysfunction; Peroxisomal dysfunction; Renal fibrosis.
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