Dmitry Namgaladze
Goethe University Frankfurt
60 Papers
390 Citations
Dmitry Namgaladze is an academic researcher from Goethe University Frankfurt. The author has contributed to research in topics: Biology & Chemistry. The author has an hindex of 22, co-authored 53 publications. Previous affiliations of Dmitry Namgaladze include University of Konstanz.
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Papers
Redox control of inflammation in macrophages.
Bernhard Brüne,Nathalie Dehne,Nina Grossmann,Michaela Jung,Dmitry Namgaladze,Tobias Schmid,Andreas von Knethen,Andreas Weigert +7 more
TL;DR: The mechanisms how redox signals add to the process of Macrophage polarization and reprogramming are summarized, how this is controlled by the interaction of macrophages with their environment, and the outcome of the polarization process in health and disease are addressed.
342
Cancer cell and macrophage cross-talk in the tumor microenvironment.
TL;DR: How hypoxia and cell death adds the cross‐talk between cancer cells and macrophages is discussed.
246
Fatty acid oxidation is dispensable for human macrophage IL-4-induced polarization
Dmitry Namgaladze,Bernhard Brüne +1 more
TL;DR: Apparently, FAO is dispensable for IL-4-induced polarization of human macrophages, pointing to fundamental differences in the metabolic requirements of macrophage phenotype alterations between mice and humans.
121
Nitration and inactivation of cytochrome P450BM‐3 by peroxynitrite
Andreas Daiber,Susanna Herold,Christian Schöneich,Dmitry Namgaladze,Julian A. Peterson,Volker Ullrich +5 more
TL;DR: Stopped-flow data presented here support the previous hypothesis that ferryl-species are involved as intermediates during the reactions of P450 enzymes with PN, and suggest an autocatalytic mechanism.
98
Antioxidant signaling via Nrf2 counteracts lipopolysaccharide-mediated inflammatory responses in foam cell macrophages.
Anne Marie Kuhn,Nico Tzieply,Martina Victoria Schmidt,Andreas von Knethen,Dmitry Namgaladze,Masayuki Yamamoto,Bernhard Brüne +6 more
TL;DR: In peritoneal FCMs from Nrf2-/- mice (C57BL/6J), the LPS-induced proinflammatory response was restored and the cells to regain a proinflammatory phenotype, Mechanistically, oxLDL attenuated ROS-dependent activation of CCAAT/enhancer binding protein (C/EBP) family members in FCMs, thereby reducing cytokine expression.
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