Role of abnormal sarcoplasmic reticulum function in atrial fibrillation

    Therapy (London, England : 2004)
    |September 28, 2011
    PubMed

    Insights

    Atrial fibrillation (AF) involves altered calcium handling in the heart's upper chambers, potentially causing reduced function and arrhythmias. Understanding these molecular changes offers new therapeutic targets for AF treatment.

    Area of Science:

    • Cardiology
    • Molecular Biology
    • Biochemistry

    Background:

    • Atrial fibrillation (AF) is a prevalent cardiac arrhythmia linked to substantial morbidity and mortality.
    • AF is associated with significant disruptions in sarcoplasmic reticulum calcium (Ca2+) homeostasis within atrial cells.
    • These calcium handling abnormalities may underlie both diminished contractile function and heightened arrhythmogenesis in AF.

    Purpose of the Study:

    • To review the molecular mechanisms underlying sarcoplasmic reticulum Ca2+ handling alterations in AF.
    • To explore the potential therapeutic implications of these molecular changes for managing AF.

    Main Methods:

    • Review of existing literature on AF and Ca2+ handling.
    • Analysis of studies involving human atrial tissue samples.
    • Examination of data from various animal models of AF.

    Main Results:

    • AF induces changes in the expression and posttranslational modification of key Ca2+ handling proteins.
    • These molecular alterations in Ca2+ handling are implicated in AF pathophysiology.
    • Evidence suggests a link between altered Ca2+ handling and both reduced atrial contractility and increased arrhythmia susceptibility.

    Conclusions:

    • Alterations in sarcoplasmic reticulum Ca2+ handling are a key molecular feature of AF.
    • Targeting these Ca2+ handling pathways presents a promising therapeutic strategy for AF.

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