Abstract
Copyright: © 2015 Frezza and Mauro. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Highlights
Few years ago, scientists had to struggle to convince audiences and editors that cell metabolism and biochemistry were not boring, let alone persuade the scientific community that alterations of the metabolic machinery could underpin human diseases [1]
We hear from more senior scientists that publishing the first paper on c-Myc-mediated transcriptional control of the metabolic enzyme lactate dehydrogenase as a key mechanism for cancer transformation [2] or lymphocyte survival and activation via TCR-dependent regulation of nutrient uptake and utilization [3, 4] was not easy at all
We know that signaling pathways directly control specific metabolic pathways and enzymes, and vice versa, and even more astonishingly, that intermediates of metabolism, such as lactate or succinate, or metabolic enzymes (i.e., GAPDH or PFKFB3) can regulate gene expression, protein translation, or entire processes, such as endothelial sprouting
Summary
Scientists had to struggle to convince audiences and editors that cell metabolism and biochemistry were not boring, let alone persuade the scientific community that alterations of the metabolic machinery could underpin human diseases [1]. In 2015, metabolism is the heart of an ever growing body of studies, spanning the fields of cancer, stem cells, and, as highlighted in this series of review articles, immunology and metabolic diseases.
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