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Holzerova, E. ; Prokisch, H.

Mitochondria: Much ado about nothing? How dangerous is reactive oxygen species production?

Int. J. Biochem. Cell Biol. 63, 16-20 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
For more than 50 years, reactive oxygen species have been considered as harmful agents, which can attack proteins, lipids or nucleic acids. In order to deal with reactive oxygen species, there is a sophisticated system developed in mitochondria to prevent possible damage. Indeed, increased reactive oxygen species levels contribute to pathomechanisms in several human diseases, either by its impaired defense system or increased production of reactive oxygen species. However, in the last two decades, the importance of reactive oxygen species in many cellular signaling pathways has been unraveled. Homeostatic levels were shown to be necessary for correct differentiation during embryonic expansion of stem cells. Although the mechanism is still not fully understood, we cannot only regard reactive oxygen species as a toxic by-product of mitochondrial respiration anymore.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Ros Scavenging ; Ros Signalization ; Reactive Oxygen Species; Protein-tyrosine Phosphatases; Hydrogen-peroxide; Redox Regulation; Complex Iii; Superoxide; Dehydrogenase; Thioredoxin; Inactivation; Generation; Apoptosis
Language english
Publication Year 2015
HGF-reported in Year 2015
ISSN (print) / ISBN 1357-2725
e-ISSN 1878-5875
Journal International Journal of Biochemistry & Cell Biology, The
Quellenangaben Volume: 63, Issue: , Pages: 16-20 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place Oxford
Reviewing status Peer reviewed
Institute(s) Institute of Human Genetics (IHG)
POF-Topic(s) 30501 - Systemic Analysis of Genetic and Environmental Factors that Impact Health
Research field(s) Genetics and Epidemiology
PSP Element(s) G-500700-001
PubMed ID 25666559
DOI 10.1016/j.biocel.2015.01.021
WOS ID WOS:000355710800004
Scopus ID 84939949923
Scopus ID 84923333789
Erfassungsdatum 2015-02-12
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