Fig. 10

Schematic illustration of the proposed cardioprotective mechanism of mAb A treatment in hearts following a myocardial infarction. Glucagon receptor antagonism increases the insulin signalling pathway and the BCAA catabolic pathway, while inhibiting the mTOR pathway. IRS-1 insulin receptor substrate-1, Akt protein kinase B, GSK-3β glycogen synthase kinase-3 beta, mTOR mammalian target of rapamycin, P70S6K ribosomal protein S6 kinase, AS160 Akt substrate 160, GLUT4 glucose transporter 4, PDH pyruvate dehydrogenase, TAK1 transforming growth factor beta-activated kinase 1, p38 MAPK p38 mitogen-activated protein kinase, KLF15 Krüppel-like factor 15, BCATm mitochondrial branched chain aminotransferase, BCAA branched chain amino acids, TCA tricarboxylic acid, MPC mitochondrial pyruvate carrier. Red arrows indicate the cellular changes following mAb A treatment in post-MI heart