Preservation of Post-Infarction Cardiac Structure and Function via Long-Term Oral Formyl Peptide Receptor Agonist Treatment

Preservation of Post-Infarction Cardiac Structure and Function via Long-Term Oral Formyl Peptide Receptor Agonist Treatment

Summary: Dysregulated inflammation following myocardial infarction (MI) promotes left ventricular (LV) remodeling and loss of function. Targeting inflammation resolution by activating formyl peptide receptors (FPRs) may limit adverse remodeling and progression towards heart failure. This study chara...

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Main Authors: Ricardo A. García, PhD, Bruce R. Ito, PhD, John A. Lupisella, MSc, Nancy A. Carson, BSc, Mei-Yin Hsu, MSc, Gayani Fernando, MSc, Madeleine Heroux, PhD, Michel Bouvier, PhD, Elizabeth Dierks, PhD, Ellen K. Kick, PhD, David A. Gordon, PhD, Jian Chen, PhD, Gabe Mintier, BSc, Marilyn Carrier, PhD, Stéphane St-Onge, MSc, Himanshu Shah, MSc, Jordan Towne, BSc, Marcela Sotelo Bucardo, BSc, Xiuying Ma, PhD, Carol S. Ryan, BSc, Nicholas R. Wurtz, PhD, Jacek Ostrowski, PhD, Francisco J. Villarreal, MD, PhD
Format: Article
Language:English
Published: Elsevier 2019-12-01
Series:JACC: Basic to Translational Science
Online Access:http://www.sciencedirect.com/science/article/pii/S2452302X19301962
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Summary:Summary: Dysregulated inflammation following myocardial infarction (MI) promotes left ventricular (LV) remodeling and loss of function. Targeting inflammation resolution by activating formyl peptide receptors (FPRs) may limit adverse remodeling and progression towards heart failure. This study characterized the cellular and signaling properties of Compound 43 (Cmpd43), a dual FPR1/FPR2 agonist, and examined whether Cmpd43 treatment improves LV and infarct remodeling in rodent MI models. Cmpd43 stimulated FPR1/2-mediated signaling, enhanced proresolution cellular function, and modulated cytokines. Cmpd43 increased LV function and reduced chamber remodeling while increasing proresolution macrophage markers. The findings demonstrate that FPR agonism improves cardiac structure and function post-MI. Key Words: agonist, Compound 43, formyl peptide receptor, heart failure, myocardial infarction
ISSN:2452-302X

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