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Cardioprotective effect of chronic hypoxia involves inhibition of mitochondrial permeability transition pore opening

  1. 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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