NADPH oxidase 4 contributes to oxidative stress in a mouse model of myocardial infarction
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
37159852
PubMed Central
PMC10226398
DOI
10.33549/physiolres.934992
PII: 934992
Knihovny.cz E-zdroje
- MeSH
- infarkt myokardu * genetika MeSH
- koronární cévy MeSH
- modely nemocí na zvířatech MeSH
- myši MeSH
- NADPH-oxidasa 4 * genetika MeSH
- oxidační stres * MeSH
- reaktivní formy kyslíku MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- NADPH-oxidasa 4 * MeSH
- Nox4 protein, mouse MeSH Prohlížeč
- reaktivní formy kyslíku MeSH
Oxidative stress closely related to the progression and severity of myocardial infarction (MI). Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) is one of the major enzymes that generate reactive oxygen species (ROS) in cardiovascular system. Here, we aim to elucidate the pathological role of NOX4 in MI. MI mouse model was created by the coronary artery ligation. NOX4 was specifically knocked down in heart through intramyocardial injection of siRNA. NOX4 expression and oxidative stress indicators were determined at different time points using qRT-PCR, Western blot, and ELISA, and then analyzed by Pearson's correlation. Cardiac function was evaluated by using echocardiographic technique. NOX4 was upregulated in myocardial tissues of MI mice, which positively correlated with the elevation of oxidative stress indicators. Knockdown of NOX4 in heart significantly reduced the production of ROS and the level of oxidative stress in left ventricle tissues, which was accompanied by significant improvement of cardiac function in MI mice. Selective knockdown of NOX4 in heart attenuates MI-induced oxidative stress and improves cardiac function, suggesting inhibition of NOX4/ROS axis in heart using siRNA is a potential therapeutic treatment for MI-induced cardiac dysfunction.
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