ROS Function in Redox Signaling and Oxidative Stress

Current Biology, Journal Year: 2014, Volume and Issue: 24(10), P. R453 - R462

Published: May 1, 2014

Language: Английский

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Physiological Roles of Mitochondrial Reactive Oxygen Species

Molecular Cell, Journal Year: 2012, Volume and Issue: 48(2), P. 158 - 167

Published: Oct. 1, 2012

Language: Английский

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Beyond oxidative stress: an immunologist's guide to reactive oxygen species

Nature reviews. Immunology, Journal Year: 2013, Volume and Issue: 13(5), P. 349 - 361

Published: April 25, 2013

Language: Английский

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Mitochondrial ROS Signaling in Organismal Homeostasis

Cell, Journal Year: 2015, Volume and Issue: 163(3), P. 560 - 569

Published: Oct. 1, 2015

Language: Английский

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ROS homeostasis and metabolism: a dangerous liason in cancer cells

Cell Death and Disease, Journal Year: 2016, Volume and Issue: 7(6), P. e2253 - e2253

Published: June 9, 2016

Abstract Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage genomic instability, ultimately, reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms tumors engage when faced with are critical for progression producing redox cofactors. In particular, we describe how mitochondria has key role regulating interplay between homeostasis metabolism within cells. Last, will discuss potential therapeutic use agents directly or indirectly block

Language: Английский

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Cellular adaptation to hypoxia through hypoxia inducible factors and beyond

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(5), P. 268 - 283

Published: March 6, 2020

Language: Английский

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Regulation of mammalian nucleotide metabolism and biosynthesis

Nucleic Acids Research, Journal Year: 2015, Volume and Issue: 43(4), P. 2466 - 2485

Published: Jan. 27, 2015

Nucleotides are required for a wide variety of biological processes and constantly synthesized de novo in all cells. When cells proliferate, increased nucleotide synthesis is necessary DNA replication RNA production to support protein at different stages the cell cycle, during which these events regulated multiple levels. Therefore precursor nucleotides also strongly Nucleotide an energy intensive process that uses metabolic pathways across compartments several sources carbon nitrogen. The transcription level by set master factors but enzyme allosteric regulation feedback inhibition. Here we review cellular demands biosynthesis, their mechanisms cycle. use stable isotope tracers delineating biosynthetic routes intersecting how quantitatively controlled under conditions highlighted. Moreover, importance viability discussed this may lead potential new approaches drug development diseases such as cancer.

Language: Английский

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ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection

Free Radical Biology and Medicine, Journal Year: 2018, Volume and Issue: 117, P. 76 - 89

Published: Jan. 31, 2018

Language: Английский

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Mitochondria: master regulators of danger signalling

Nature Reviews Molecular Cell Biology, Journal Year: 2012, Volume and Issue: 13(12), P. 780 - 788

Published: Nov. 23, 2012

Language: Английский

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Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs preconditioning

Redox Biology, Journal Year: 2014, Volume and Issue: 2, P. 702 - 714

Published: Jan. 1, 2014

Reductions in the blood supply produce considerable injury if duration of ischemia is prolonged. Paradoxically, restoration perfusion to ischemic organs can exacerbate tissue damage and extend size an evolving infarct. Being highly metabolic organs, heart brain are particularly vulnerable deleterious effects ischemia/reperfusion (I/R). While pathogenetic mechanisms contributing I/R-induced infarction multifactorial, relative importance each factor remains unclear. However, emerging body evidence indicates that generation reactive oxygen species (ROS) by mitochondria plays a critical role damaging cellular components initiating cell death. In this review, we summarize our current understanding whereby mitochondrial ROS occurs I/R contributes myocardial stroke. addition, have been shown participate preconditioning several pharmacologic agents target potassium channels (e.g., ATP-sensitive (mKATP) or large conductance, calcium-activated (mBKCa) channels) activate survival programs render tissues more resistant I/R. Finally, review novel therapeutic approaches selectively mROS production reduce postischemic injury, which may prove efficacious limiting dysfunction abrogating neurocognitive deficits neuronal death

Language: Английский

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