It is now clear that altering flux through specific metabolic pathways, without changing bioenergetic rates per se, can have substantial impacts on physiological and disease processes as varied as oncogenesis, heart failure, immune cell activation, and neuronal excitability. Our work seeks to understand how shifting the nutrient preference away from oxidation of glucose and towards that of amino acids, fatty acids, and ketone bodies can adjust cell and tissue physiology in the context of neurodegeneration and heart failure.
Related Publications
Divakaruni AS, Wallace M, Buren C, Martyniuk K, Andreyev AY, Li E, Fields JA, Cordes T, Reynolds IJ, Bloodgood BL, Raymond LA, Metallo CM, and Murphy AN (2017) Inhibition of the mitochondrial pyruvate carrier protects from excitotoxic neuronal death. Journal of Cell Biology. 216(4):1091-105. 28254829
Vacanti NM, Divakaruni AS, Green CR, Parker SJ, Henry RR, Ciaraldi TP, Murphy AN, and Metallo CM (2014) Regulation of substrate utilization by the mitochondrial pyruvate carrier. Molecular Cell. 56(3):425-35. 25458843
Divakaruni AS, Wiley SE, Rogers GW, Andreyev AY, Petrosyan S, Loviscach M, Wall EA, Yadava N, Heuck AP, Ferrick DA, Henry RR, McDonald WG, Colca JR, Simon MI, Ciaraldi TP, and Murphy AN (2013) Thiazolidinediones are acute, specific inhibitors of the mitochondrial pyruvate carrier. Proceedings of the National Academy of Sciences, USA. 110(14):5422-7. 23513224
