Myokine Musclin Is Critical for Exercise-Induced Cardiac Conditioning

January 1, 2023
Int J Mol Sci
https://pubmed.ncbi.nlm.nih.gov/37047496

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/37047496

Research summary

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.

Key outcome of the study

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.

Mouse model

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.

TARGET:
Ostn
Osteocrin, Musclin

Keywords

Cardioprotection, Exercise physiology, Mitochondrial biogenesis, Myokines, cGMP signaling

Technical specifications

Constitutive Knockout model, Exon 2 deletion, Homologous recombination, C57BL/6N background, Synthetic peptide infusion studies

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