A novel peptide improving cardiac function post-myocardial infarction in CKD

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A novel peptide improving cardiac function post-myocardial infarction in CKD

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Co-author 1

Adelina Curaj Curaj@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany -

Co-author 2

Vera Jankowski vjankowski@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany -

Co-author 3

Joachim Jankowski jjankowski@ukaachen.de RWTH University Institute for Molecular Cardiovascular Research Aachen Germany *

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Introduction

Extensive scar formation following myocardial infarction (MI) has a negative impact on cardiac function, thus promoting heart failure development. Therefore, therapies limiting scar formation post-MI are highly needed.

Methods

Mice subjected to chronic ligation of the left anterior descending coronary artery were treated with VIF applied subcutaneously for two weeks post-MI and then analyzed at different time points in vivo and ex vivo.

Results

VIF treatment resulted in a lower mortality rate (20%) compared to the saline-treated group (60%). In addition, VIF treatment improved left ventricular ejection fraction and reduced myocardial scar size compared to control mice. Moreover, VIF-treatment influenced the extracellular matrix composition by increasing collagen-5 content in the myocardial scar tissue andupregulating collagen-5 gene expression. Furthermore, VIF treatment led to upregulation of conditioning genes with protective effects against hypoxia-induced injury, such as HIF-1α and HMOX-1, as well as anti-apoptotic gene BCL-2 in AC16 cardiomyocytes, compared to control cells. Finally, patients with ACS exhibited increased VIF plasma levels compared to healthy subjects, raising the hypothesis of a compensatory effect of VIP to prevent end-organ damage.

Conclusion

Following myocardial infarction, VIF treatment provides cardioprotection through two key mechanisms: (i) VIF activates conditioning genes such as HIF-1α and HMOX-1, helping cardiomyocytes survive hypoxic injury as an adaptive response, and (ii) VIF modulates extracellular matrix composition which reduces scar size and therefore improves the left ventricular ejection fraction.

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