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A Worm-to-Man Survey of Physiological and Pathophysiological Aspects Thomas A. Gorr (University of Zürich, Switzerland) The hypoxia-inducible transcription factor (HIF) has been described as key mediator for transducing changes in [O2] onto DNA level from 'worms' (C. elegans), to flies (Drosophila), to fish (teleosts) and mammals. Surprisingly enough, HIF-driven gene regulations in response to acute and chronic deprivations of oxygen are also of central importance, despite markedly different physiological outcomes, in hypoxia-tolerant and -sensitive tissues or animals alike. Several disease states, e.g. cancer, are, compared to healthy tissue, commonly aggravated by hyperactive HIF signaling in association with a far more stress or treatment resistant and aggressive phenotype. Therefore, novel HIF functions and control mechanisms, which not only endow cells to withstand and recover from severe hypoxia but also keep the activity of this transcription factor within physiological limits, are becoming increasingly important research aspects in the field. O2 sensing via HIF has obviously begun to link historically independent trajectories between comparative and clinically applied biology into a far more coherent, unifying outlook on hypoxia-mediated cellular adaptations. To continue down this integrative path, our symposium aims to explore cellular and organismal adaptations to hypoxia, as conferred by the HIF signaling pathway, in a comparative manner. We also invite ideas and insights from invertebrate and vertebrate animal models that might apply to study or manipulate HIF signaling in human disease.
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