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Ivan I. Galkin

Researcher at Moscow State University

Publications -  27
Citations -  403

Ivan I. Galkin is an academic researcher from Moscow State University. The author has contributed to research in topics: Medicine & Endothelium. The author has an hindex of 9, co-authored 21 publications receiving 252 citations.

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Mitochondrial reactive oxygen species are involved in chemoattractant-induced oxidative burst and degranulation of human neutrophils in vitro

TL;DR: Data indicate that mtROS play a critical role in signal transduction that mediates the major neutrophil functional responses in the process of activation, and is implicated in the oxidative burst caused by NOX2 activation as well as in the exocytosis of primary and secondary granules.
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Role of mitochondrial reactive oxygen species in age-related inflammatory activation of endothelium

TL;DR: The data indicate an important role of mitochondrial reactive oxygen species in regulation of the NF-κB pathway and corresponding age-related inflammatory activation of endothelium.
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Mitochondrial permeability transition pore is involved in oxidative burst and NETosis of human neutrophils.

TL;DR: It is shown that both sources of ROS, mitochondria and NADPH oxidase, are involved in NETosis induced by A23187 in human neutrophils and the mPTP is involved in mtROS production, NETosis, and the oxidative burst induced by a23187.
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Low concentration of uncouplers of oxidative phosphorylation decreases the TNF-induced endothelial permeability and lethality in mice.

TL;DR: In vitro mild uncoupling rescued from TNF-induced endothelial permeability, disassembly of cell contacts and VE-cadherin cleavage by the matrix metalloprotease 9, suggesting that the protective action of the uncouplers is linked to their antioxidant potential.
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Age-associated murine cardiac lesions are attenuated by the mitochondria-targeted antioxidant SkQ1.

TL;DR: The data indicate a causative role of mitochondrial reactive oxygen species in cardiovascular aging and imply that SkQ1 has potential as a drug against age-related cardiac dysfunction.