The role of PFKFB3 in renal brosis

Persistently elevated glycolysis in kidney has been demonstrated to promote chronic kidney disease. However, the underlying mechanism remains largely unclear. Here, we observed that PFKFB3, a key glycolytic enzyme, was remarkably induced in kidney proximal tubular cells following ischemia-reperfusion injury in mice, as well as in multiple etiologies of chronic kidney disease patients. PFKFB3 expression was positively correlated with the severity of renal fibrosis. Proximal tubular epithelial-specific deletion of PFKFB3 significantly reduced renal lactate levels, mitigated inflammation and fibrosis, and preserved renal function in the IRI mouse model. Targeting PFKFB3-mediated inflammation activation in tubular cells could be a novel strategy for chronic kidney disease therapy.