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Acute myocardial infarction (MI) is a leading cause of death worldwide. Although with current treatment, acute mortality from MI is low, the damage and remodeling associated with MI are responsible for subsequent heart failure. Reducing cell death associated with acute MI would decrease the mortality associated with heart failure.

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The close interaction of mitochondrial fission and mitophagy, two crucial mechanisms, is key in the progression of myocardial ischemia-reperfusion (IR) injury. However, the upstream regulatory mechanisms governing these processes remain poorly understood. Here, we demonstrate a marked elevation in Nr4a1 expression following myocardial IR injury, which is associated with impaired cardiac function, heightened cardiomyocyte apoptosis, exacerbated inflammatory responses, and endothelial dysfunction.

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Myocardial injury is prone to occur during myocardial ischemia-reperfusion, which further causes adverse cardiac events. Cardiomyopeptide (CMP) has been found to protect the heart against ischemia-reperfusion injury. The present study will explore the molecular and signaling mechanisms associated with the therapeutic effects of CMP.

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Left bundle branch block - innocent bystander, silent menace, or both.

Heart Rhythm

December 2024

Christian-Albrechts-University, Medical Faculty, Christian-Albrechts-Platz 4, 24118 Kiel, Germany; University of Applied Science, Life Sciences, An der Karlstadt 8, 27568 Bremerhaven, Germany. Electronic address:

Left bundle branch block (LBBB) causes immediate electrical and mechanical dys-synchrony of the left ventricle (LV) and gradual structural damages in the Purkinje cells and myocardium. Mechanical dys-synchrony reduces the LV ejection fraction (EF) instantly, but only to ≈55% in an otherwise normal heart. Because of the heart's in-built functional redundancy, a patient with LBBB does not always notice the heart's reduced efficiency straight away.

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Methomyl (MET), a universally used insecticide, has many adverse effects on various organs in both humans and animals including the liver, kidneys, and heart. Betaine (BET), a natural antioxidant, has a protective role against many toxicants-induced cardiovascular disorders. The present study was designed to elucidate the molecular mechanistic way underlying the mitigating effect of BET against MET-induced cardiopulmonary injury and inflammation in rats.

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