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    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Cardiology

    Background:

    • Tafazzin is a mitochondrial enzyme crucial for phospholipid remodeling.
    • Mutations in tafazzin cause Barth syndrome, characterized by cardiomyopathy.
    • Tafazzin deficiency leads to altered cardiolipin (CL) acyl chains, reduced CL levels, and monolysocardiolipin (MLCL) accumulation.

    Purpose of the Study:

    • To investigate the impact of tafazzin deficiency on cardiac phospholipid composition, particularly plasmalogens.
    • To elucidate the role of plasmenylcholine in tafazzin-mediated cardiolipin remodeling in the heart.

    Main Methods:

    • High-resolution 31P nuclear magnetic resonance (NMR) with cryoprobe technology to analyze phospholipid composition in tafazzin-knockdown (TAZ-KD) mouse hearts.
    • Quantitative Western blot to assess protein expression levels, including peroxisomal enzymes.

    Main Results:

    • TAZ-KD hearts showed decreased CL (6.4% to 2.0%) and increased MLCL (undetected to 3.3%).
    • A significant reduction in plasmenylcholine (30.8% to 18.1%) was observed in TAZ-KD hearts.
    • Far1 enzyme expression, critical for plasmalogen synthesis, was upregulated 8.3-fold in TAZ-KD models.
    • Lyso-plasmenylcholine and plasmenylcholine were identified as substrates for tafazzin in transacylation reactions.

    Conclusions:

    • Tafazzin deficiency profoundly affects cardiac plasmenylcholine levels.
    • Plasmenylcholine, particularly linoleoyl species, plays a vital role in cardiolipin remodeling within the heart.
    • The observed changes in plasmenylcholine contribute to the cardiac dysfunction seen in Barth syndrome.