Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/00216208:11130/25:10499315

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Involvement of Oxidative Stress in Mitochondrial Abnormalities During the Development of Heart Disease

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30201 - Cardiac and Cardiovascular systems

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2025

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Biomedicines

ISSN

2227-9059

e-ISSN

2227-9059

Svazek periodika

13

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

22

Strana od-do

1338

Kód UT WoS článku

001518020900001

EID výsledku v databázi Scopus

2-s2.0-105008985582