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Cardioprotective effect of chronic hypoxia involves inhibition of mitochondrial permeability transition pore opening
- 1.0602157 - FGÚ 2025 RIV CZ eng J - Článek v odborném periodiku
Alánová, Petra - Alán, Lukáš - Neckář, Jan - Ošťádal, Bohuslav - Kolář, František
Cardioprotective effect of chronic hypoxia involves inhibition of mitochondrial permeability transition pore opening.
Physiological Research. Roč. 73, č. 5 (2024), s. 881-885. ISSN 0862-8408. E-ISSN 1802-9973
Grant CEP: GA MŠMT(CZ) LX22NPO5104; GA MZd(CZ) NU20J-02-00035
Institucionální podpora: RVO:67985823
Klíčová slova: cardioprotection * chronic hypoxia * mitochondria * permeability transition pore * myocardial infarction
Obor OECD: Cardiac and Cardiovascular systems
Impakt faktor: 1.9, rok: 2023 ; AIS: 0.393, rok: 2023
Způsob publikování: Open access
Web výsledku:
https://www.biomed.cas.cz/physiolres/pdf/2024/73_881.pdf
DOI: https://doi.org/10.33549/physiolres.935427
The aim of the study was to examine the potential role of mitochondrial permeability transition pore (mPTP) in the cardioprotective effect of chronic continuous hypoxia (CH) against acute myocardial ischemia/reperfusion (I/R) injury. Adult male Wistar rats were adapted to CH for 3 weeks, while their controls were kept under normoxic conditions. Subsequently, they were subjected to I/R insult while being administered with mPTP inhibitor, cyclosporin A (CsA). Infarct size and incidence of ischemic and reperfusion arrhythmias were determined. Our results showed that adaptation to CH as well as CsA administration reduced myocardial infarct size in comparison to the corresponding control groups. However, administration of CsA did not amplify the beneficial effect of CH, suggesting that inhibition of mPTP opening contributes to the protective character of CH.
Trvalý link: https://hdl.handle.net/11104/0359366
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