Fig. 9 | Signal Transduction and Targeted Therapy

Fig. 9

From: Suppression of PFKFB3-driven glycolysis restrains endothelial-to-mesenchymal transition and fibrotic response

Fig. 9

Schematic depicting the molecular mechanism through which SAC restrains EndoMT via suppression of PFKFB3. EndoMT is characterized by increased expression of PFKFB3 that drives abnormal glycolysis and hijacks glucose flux from pentose phosphate pathway (PPP) to compromise cytoplasmic NADPH production. Efflux of mitochondrial NADPH through isocitrate/α-KG shuttle replenishes cytoplasmic NADPH pool but meanwhile impairs mitochondrial respiration by hampering mitochondrial Fe-S cluster protein biosynthesis. SAC disrupts PFKFB3 stability by accelerating its degradation and thus maintains endothelial metabolic homeostasis, underlying its anti-EndoMT effects

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