myocardial infarction

[Scientific Reports] The authors demonstrated that entricular tachycardias susceptibility in the chronic phase after myocardial infarction was reduced in mice with cardiomyocyte-specific β-catenin deletion primarily through attenuated structural remodeling, but not ion channel gene alterations.

[Cell Death & Disease] Rat cardiomyocyte cell line H9C2 and primary rat cardiac fibroblasts were cultured in conditioned media generated from epicardial adipose tissue (EAT) of rats in the myocardial infarction 4-week group (EAT-CM). Functionally, EAT-CM enlarged the cell surface area of H9C2 cells and reinforced cardiac fibroblast activation into myofibroblasts by elevating intracellular reactive oxygen species levels.

[Experimental and Molecular Medicine] Researchers found that cytochrome c oxidase subunit 5a expression was noticeably decreased in myocardial infarcted rat hearts and myocardial cells under hypoxic conditions, regulated other identified proteins and was closely related to hypoxia-induced cell death.

[Stem Cell Reports] Investigators used a porcine model to provide proof-of-concept evidence that a combination of amiodarone and ivabradine could effectively suppress engraftment arrhythmia.

[Circulation Research] Using LysMCre-mediated mammalian STE20-like protein kinase 1/2 (Mst1/2)-deficient mice, researchers found that MST1 deficiency exacerbated cardiac dysfunction after myocardial infarction.

[Biology Open] The author provides a critical perspective about the main mechanisms contributing to regulate cellular crosstalk in the heart, which may be considered in the development of future therapeutic strategies, using cell-based therapies as a paradigmatic example.