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Abstract
ANXA2 was highly expressed in murine and human ischemic failing hearts, with increased circulating ANXA2 positively correlating with cardiac injury in patients with acute myocardial infarction.
- Cardiomyocyte-specific depletion of ANXA2 prevented inactivation of cardiac mitophagy, oxidative stress, cell death, and inflammatory infiltration after myocardial infarction.
- This depletion led to significant improvements in infarct size, heart function, and cardiac remodeling.
- Overexpression of ANXA2 in cardiomyocytes suppressed mitophagy, worsening cardiac injury and heart failure following myocardial infarction.
- ANXA2 was found to interact directly with the mitophagy receptor PHB2, blocking the binding of another protein, LC3B, to PHB2 and promoting its degradation.
- Silencing PHB2 negated the protective effects of ANXA2 deficiency on mitochondrial function and cell viability in stressed myocytes.
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