About this Research Topic
The Research Topic’s scope is to gather submissions focusing on the broad spectrum of hypoxia-induced metabolic changes as a driving factor for subsequent intracellular and whole-body changes ranging from the development of type 2 diabetes (impaired insulin sensitivity, β-cell dysfunction) to modified regulation of cell cycle and cancer pathogenesis and progression. Anticipated papers will include research on metabolic shifts affecting the fate of carbohydrates, lipids and amino-acids together with appropriate intermediates as well as experimental work describing mitochondrial structural and functional adaptations, Krebs cycle modifications, or consequences of reductive glutamine carboxylation (including molecular mechanisms mediating such metabolic modifications) as well as any other aspect of research linking oxygen availability and metabolic functions. Research using multiple cutting-edge methodological approaches at the level ranging from single cell to the whole organism (animal or human) is welcomed. Research focusing on the role of well established intracellular signalling (e.g. HIF-dependent pathways), reactive oxygen species generation, transcriptional regulation as well as investigating possible novel pathways and targets is desired.
All formats of contributions (original research papers, opinions, full reviews, mini-reviews) will be considered. Basic research at the cellular or sub-cellular level, translational research using animal experiments and human physiological as well as epidemiological or interventional studies are expected.
Keywords: hypoxia, Krebs cycle, hypoxia-inducible factor, oxygen, glutamin, reductive glutamine carboxylation, cancer, isocitrate dehydrogenase, citrate
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.