Research interests and know-how
Organ failure after severe trauma or infection is a serious consequence in critical care patients, often leading to death. The mechanisms causing this life threatening complication remain to be determined. What role reactive oxygen and nitrogen species play in this process is currently an exciting question. Particular attention is given to signalling pathways regulated by mitochondria.
I am addressing this question through application of mitochondria-targeted antioxidants in different models (fresh tissue slices, primary cells, cell lines,…). These experimental models include local and systemic inflammatory response, ischemia-reperfusion injury and shock. The major methods used are (i) high resolution respirometry (Oroboros Instruments 2k), (ii) electron paramagnetic resonance spectroscopy (Magnettech Miniscope MS200), (iii) confocal microscopy (Zeiss LSM510) and (iv) isolation of subcellular organelles e.g. mitochondria.
More recently, research interest was extended to mechanisms underlying stem cell activation. The focus of this study is on therapeutically relevant human stem cells from “clinical waste materials” such as amnion or adipose tissue. My near-term goals are thus to investigate the role of mitochondria and reactive oxygen species in metabolic pathways involved in the activation of stem cells, in order to optimise the activation of stem cells for diagnostic and therapeutic approaches.
Selected Publications
Weidinger A, Birgisdóttir L, Schäffer J, Meszaros AT, Zavadskis S, Müllebner A, Hecker M, Duvigneau JC, Sommer N, Kozlov AV (2022) Systemic Effects of mitoTEMPO upon Lipopolysaccharide Challenge Are Due to Its Antioxidant Part, While Local Effects in the Lung Are Due to Triphenylphosphonium. Antioxidants. 2022 Feb 6;11 (2): 323.
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Kozlov AV, Lancaster JR Jr, Meszaros AT, Weidinger A (2017). Mitochondria-meditated pathways of organ failure upon inflammation. Redox Biol,13:170-181
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Weidinger A & Kozlov AV (2015). Biological activities of reactive oxygen and nitrogen species: oxidative stress versus signal transduction. Biomolecules, 5(2):472-484.
(free PDF)