Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F25%3A10499315" target="_blank" >RIV/00064203:_____/25:10499315 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11130/25:10499315
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=8drorBT79Q" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=8drorBT79Q</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/biomedicines13061338" target="_blank" >10.3390/biomedicines13061338</a>
Alternative languages
Result language
angličtina
Original language name
Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease
Original language description
Background: Several mitochondrial abnormalities such as defective energy production, depletion of energy stores, Ca(2+) accumulation, generation of reactive oxygen species, and impaired intracellular signaling are associated with cardiac dysfunction during the development of different heart diseases. Methods: A narrative review was compiled by a search for applicable literature in MEDLINE via PubMed. Results: Mitochondria generate ATP through the processes of electron transport and oxidative phosphorylation, which is used as energy for cardiac contractile function. Mitochondria, in fact, are the key subcellular organelle for the regulation of intracellular Ca(2+) concentration and are considered to serve as a buffer to maintain Ca(2+) homeostasis in cardiomyocytes. However, during the development of heart disease, the excessive accumulation of intracellular Ca(2+) results in mitochondria Ca(2+)-overload, which, in turn, impairs mitochondrial energy production and induces cardiac dysfunction. Mitochondria also generate reactive oxygen species (ROS), including superoxide anion radicals and hydroxyl radicals as well as non-radical oxidants such as hydrogen peroxide, which promote lipid peroxidation and the subsequent disturbance of Ca(2+) homeostasis, cellular damage, and death. Conclusion: These observations support the view that both oxidative stress and intracellular Ca(2+)-overload play a critical role in mitochondrial disruption during the pathogenesis of different cardiac pathologies.
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
30201 - Cardiac and Cardiovascular systems
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Biomedicines
ISSN
2227-9059
e-ISSN
2227-9059
Volume of the periodical
13
Issue of the periodical within the volume
6
Country of publishing house
CH - SWITZERLAND
Number of pages
22
Pages from-to
1338
UT code for WoS article
001518020900001
EID of the result in the Scopus database
2-s2.0-105008985582