Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00493119" target="_blank" >RIV/67985823:_____/18:00493119 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1089/ars.2017.7225" target="_blank" >http://dx.doi.org/10.1089/ars.2017.7225</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1089/ars.2017.7225" target="_blank" >10.1089/ars.2017.7225</a>
Alternative languages
Result language
angličtina
Original language name
Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling
Original language description
Significance: Mitochondria are the energetic, metabolic, redox, and information signaling centers of the cell. Substrate pressure, mitochondrial network dynamics, and cristae morphology state are integrated by the protonmotive force Delta p or its potential component, Delta Psi , which are attenuated by proton backflux into the matrix, termed uncoupling. The mitochondrial uncoupling proteins (UCP1-5) play an eminent role in the regulation of each of the mentioned aspects, being involved in numerous physiological events including redox signaling. Recent Advances: UCP2 structure, including purine nucleotide and fatty acid (FA) binding sites, strongly support the FA cycling mechanism: UCP2 expels FA anions, whereas uncoupling is achieved by the membrane backflux of protonated FA. Nascent FAs, cleaved by phospholipases, are preferential. The resulting Delta p dissipation decreases superoxide formation dependent on Delta p. UCP-mediated antioxidant protection and its impairment are expected to play a major role in cell physiology and pathology. Moreover, UCP2-mediated aspartate, oxaloacetate, and malate antiport with phosphate is expected to alter metabolism of cancer cells. Critical Issues: A wide range of UCP antioxidant effects and participations in redox signaling have been reported, however, mechanisms of UCP activation are still debated. Switching off/on the UCP2 protonophoretic function might serve as redox signaling either by employing/releasing the extra capacity of cell antioxidant systems or by directly increasing/decreasing mitochondrial superoxide sources. Rapid UCP2 degradation, FA levels, elevation of purine nucleotides, decreased Mg2+, or increased pyruvate accumulation may initiate UCP-mediated redox signaling. Future Directions: Issues such as UCP2 participation in glucose sensing, neuronal (synaptic) function, and immune cell activation should be elucidated.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Antioxidants & Redox Signaling
ISSN
1523-0864
e-ISSN
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Volume of the periodical
29
Issue of the periodical within the volume
7
Country of publishing house
US - UNITED STATES
Number of pages
48
Pages from-to
667-714
UT code for WoS article
000439467100004
EID of the result in the Scopus database
2-s2.0-85044749273