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It is our intention to elucidate biochemical signatures with relevance to inflammation and hypoxia, thus contributing to Biomedical Research in the area of pathophysiological signal transduction (pathobiochemistry).
Our research interests center on physiological/pathophysiological signal transduction pathways of stress components, which are relevant for the comprehension of human disease. Specifically, we aim at understanding: (1) Inflammation associated with malfunctions in oxygen metabolism (2) Tumor biology linked to macrophage polarization and lipid metabolism (3) Hypoxia /HIF-1α and HIF-2α (hypoxia inducible factor-1α/2α) and its role in biomedicine (4) Molecular mechanisms in sepsis development and progression.
Various types of cellular stress such as redox-changes, a lack of oxygen (hypoxia), inflammation and/or cell demise promote cell damage, repair or adaptation towards growth as well as differentiation. Endogenous defense mechanisms balance cell or tissue injury to allow progression towards healing, anti-inflammatory outcomes and cell survival. Understanding cell destructive pathways appears to be of considerable importance in proposing therapeutic means for areas in biomedicine when oxygen supply to cells/tissues becomes limiting (hypoxia/ischemia), during cancer, when macrophage polarization affects tumor biology, and when modulation of innate immunity is required to balance pro- vs. anti-inflammatory signals.
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