myocardial infarction

[Idorsia Pharmaceuticals Ltd] Idorsia Pharmaceuticals Ltd announced the initiation of the Phase III registration study “SOS-AMI” to evaluate the efficacy and safety of self-administered subcutaneous selatogrel, Idorsia’s P2Y12 receptor antagonist, in suspected acute myocardial infarction.

[Nature Communications] Using single-cell RNA sequencing, scientists delineated the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure.

[Acta Pharmacologica Sinica] Expression of an IDH2 mutant mimicking deacetylation in cardiomyocytes promoted myocardial IDH2 activation, quenched mitochondrial reactive oxygen species (ROS), and alleviated post-myocardial infarction (MI) injury, whereas expression of an acetylation mimic in cardiomyocytes inactivated IDH2, exacerbated mitochondrial ROS overload, and aggravated post-MI injury.

[Scientific Reports] Investigators developed a mouse model in which a mutated form of HIF1α could be inducibly expressed in cardiomyocytes, and suggested that loss of calcium/calmodulin dependent protein kinase II, gamma (CAMK2G) after myocardial infarction was HIF1-dependent and may have played an important role in the heart’s calcium signaling and response to hypoxia.

[Cytotherapy] The available evidence concerning umbilical cord-derived MSCs in acute myocardial infarction is reviewed, focusing on large animal pre-clinical studies and early human trials.

[Scientific Reports] The authors conducted exploratory factor analysis to examine the interrelationships between ECM biomarkers, and cluster analysis to identify if distinct ECM profiles could distinguish patient risk in acute myocardial infarction.