Mitochondrial Antiviral Signaling Protein (MAVS) in Post-MI Cardiac Remodeling

Abstract

Background: Mitochondrial Antiviral Signaling Protein (MAVS) is an innate immune effector protein uniquely residing on mitochondrial surfaces. Previously, we identified MAVS as a key regulator of cardiac remodeling, inflammation, and metabolism in murine models of pressure-induced heart failure. This current study investigates MAVS in myocardial infarction (MI), hypothesizing a key role in cardiac stress responses. Methods: Utilizing left anterior descending artery (LAD) ligation, we induced MI in Mavs⁻ᐟ⁻ and WT mice to assess remodeling, function, and molecular changes. Results: Male Mavs⁻ᐟ⁻ mice exhibited reduced MI-induced hypertrophy, preserved ejection fraction, and diminished heart failure markers compared to WT controls. Several notable sex-based variations indicate MAVS functions in a sex-specific context. Impact: Our findings indicate that MAVS may be a critical regulator of cardiac hypertrophy and remodeling post-MI. This research underscores the potential for targeting mitochondrial activity-based pathways to improve post-MI cardiac remodeling, with MAVS as a possible candidate.