Fig. 8: The role of podocytes BCAAs catabolic defects upon DKD progression. | Nature Communications

Fig. 8: The role of podocytes BCAAs catabolic defects upon DKD progression.

From: Branched-chain amino acids contribute to diabetic kidney disease progression via PKM2-mediated podocyte metabolic reprogramming and apoptosis

Fig. 8

Glomerular podocytes in male and female patients with DKD and db/db mice specifically display BCAA catabolic defects. BCAA catabolic defects contribute to DKD development by inducing renal podocyte metabolic remodeling and apoptosis. BCAA catabolic defects result in podocyte PKM2 depolymerization and inactivation, which inhibits glucose OXPHOS and promotes a shift in glucose metabolism to serine biosynthesis and folate metabolism. BCAA promotes PKM2-DDIT3 binding, nuclear co-transportation, and regulates DDIT3 transcriptional activation of Chac1 and Trib3, which induce podocyte apoptosis.

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