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[Signaling mechanism of cardioprotective effects of opioids]

L N Maslov, L Hanus, J -M Pei

    Eksperimental'Naia I Klinicheskaia Farmakologiia
    |June 18, 2013
    PubMed

    Insights

    Opioids protect the heart by activating specific signaling pathways involving various kinases and receptors. These mechanisms are crucial for developing cardiac tolerance to ischemia and reperfusion injury.

    Area of Science:

    • Cardiovascular Pharmacology
    • Molecular Cardiology
    • Signal Transduction

    Background:

    • G(i/o)-proteins mediate intracellular signaling between opioid receptors and protein kinases.
    • Opioids exert significant cardioprotective effects through complex molecular pathways.

    Purpose of the Study:

    • To elucidate the specific protein kinases and signaling cascades involved in the cardioprotective effects of opioids.
    • To investigate the role of receptor transactivation in opioid-induced cardiac tolerance.

    Main Methods:

    • Investigated the involvement of protein kinase C, PI3 kinase, Akt, MEK1/2, ERK1/2, Src, JAK2, JNK, p70s6K, and GRK2.
    • Examined the role of nitric oxide synthase (NO-synthase).
    • Studied the transactivation of opioid, adenosine, and EGF receptors.

    Main Results:

    • Protein kinase C mediates anti-necrotic and anti-apoptotic effects of opioids.
    • PI3 kinase, Akt, MEK1/2, ERK1/2, Src, and JAK2 are involved in opioid-induced cardioprotection.
    • Opioid transactivation of EGF receptors links opioid receptors to ERK1/2 and PI3 kinase signaling.

    Conclusions:

    • Multiple kinase pathways and receptor transactivation are critical for opioid-mediated cardioprotection and cardiac tolerance.
    • Further research is needed on JNK, p70s6K, and GRK2 in opioid-induced cardiac tolerance.
    • NO-synthase plays a key role in the cardioprotective action of opioids.

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