Special Issue "Gene Regulation by HIFs during Hypoxia"
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 31 December 2018
Exposure of human cells and/or tissues to low oxygen conditions, which is termed hypoxia, characterizes healthy activities, such as intense muscular exercise and living at high altitudes, as well as many pathological conditions, including pulmonary diseases, ischemia, inflammatory disorders and cancer. Adaptation to hypoxic conditions requires dramatic changes in gene expression, orchestrated by the hypoxia inducible transcription factors HIF-1 and HIF-2.
Since the first break-through identification of HIF-1 in 1995 by Semenza and co-workers, we have learned a great deal, both about the mechanisms that regulate HIFs in response to oxygen concentration changes, and about HIF target genes, the products of which mediate metabolic reprogramming, angiogenesis, erythropoiesis and many other homeostatic changes that allow adaptation to hypoxia or lead to apoptosis and cell death under extreme lack of oxygen. These findings have established HIFs as major players in both health and disease and triggered a world-wide effort to find ways of controlling their activity for therapeutic purposes.
Investigations of single gene expression as well as genome-wide studies have shown that HIFs bind to a short consensus sequence termed Hypoxia Response Element (HRE). However, HREs are much more abundant in the human genome than the number of true HIF gene targets, making their prediction impossible and necessitating non-trivial experimental verification. In this respect, characterization of the genes directly regulated by hypoxia is an ongoing process, which continues to provide important information on the cellular pathways affected by hypoxia and their role in the hypoxic response. As drugs that target HIFs either as inhibitors, in the case of cancer, or as stimulants, in the case of defective erythropoiesis, have recently been developed and may soon enter the market, it becomes imperative to produce a full inventory of the genes, the expression of which is affected when HIF activity is modulated by medicinal agents.
Furthermore, the molecular/structural details and tissue or isoform specificity of the oxygen-dependent and oxygen-independent mechanisms that fine-tune HIF activity, control the choice of common or distinct HIF targets and affect the interaction of HIFs with chromatin and the transcriptional machinery are still a matter of intense investigation. Full delineation of these mechanisms and their spatio-temporal coordination can offer additional possibilities to artificially influence HIF-dependent gene expression as means for treating a disease.
Prof. George Simos
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