This study investigates the role of the myokine musclin in exercise-induced cardiac protection. Using Ostn<sup>−/−</sup> mice, researchers demonstrate that the absence of musclin abolishes the cardioprotective effects of exercise, including reduced infarct size and enhanced mitochondrial function. Synthetic musclin infusion restores these benefits, highlighting musclin's essential role in mediating exercise-induced cardiac conditioning.
Musclin is essential for exercise-induced cardioprotection, facilitating mitochondrial biogenesis and function through cGMP/PKG/CREB/PGC1α signaling pathways. Its absence negates the benefits of exercise on cardiac ischemic resistance, which can be restored via synthetic musclin infusion.
Ostn −/− (musclin Knockout) mouse model developed by genOway, featuring a 2.1-kb deletion flanking exon 2 of the Ostn gene, resulting in the inactivation of musclin expression.
Cardioprotection, Exercise physiology, Mitochondrial biogenesis, Myokines, cGMP signaling
Constitutive Knockout model, Exon 2 deletion, Homologous recombination, C57BL/6N background, Synthetic peptide infusion studies
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