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. Author manuscript; available in PMC: 2018 Dec 28.
Published in final edited form as: Circ Res. 2018 Jan 4;122(5):730–741. doi: 10.1161/CIRCRESAHA.117.312422

Figure 7. Model for reprogrammed hepatic metabolism by (pro)renin receptor ([P]RR) inhibition.

Figure 7.

Inhibiting hepatic (P)RR reduces PDH (pyruvate dehydrogenase) activity, impairing pyruvate metabolism and reducing acetyl-CoA supply from pyruvate, which limits fatty acid (FA) biosynthesis. (P)RR inhibition further limits FA biosynthesis by reducing protein abundance of ACC (acetyl-CoA carboxylase), the crucial enzyme in FA biosynthesis. It further signals to increase FA oxidation via reduced malonyl-CoA, an inhibitor of FA oxidation that blocks the transportation of long-chain fatty acylcarnitine by carnitine acyltransferase I (CAT1). TCA indicates tricarboxylic acid.