myocardial infarction

[Molecular Medicine Reports] Scientists investigated the involvement of Interferon regulatory factor (IRF) 2 in myocardial infarction (MI) and the underlying mechanism of IRF2 in pyroptosis. To mimic MI, ligation of the left anterior descending coronary artery was performed to establish an in vivo mouse model and rat cardiomyocytes H9c2 cells were cultured under hypoxic conditions to establish an in vitro model.

[Molecular Therapy-Nucleic Acids] Using unbiased transcriptome profiling of hypoxia-preconditioned MSCs and normoxic MSCs, scientists identified a lncRNA named lung cancer-associated transcript 1 (LUCAT1) under hypoxia.

[Biomedical Journal] Scientists probed into the role and the underlying regulatory mechanism of apoptosis-inducing factor mitochondria associated 1 (AIFM1) in myocardial injury.

[Hypertension Research] Hypoxia increased α1-AR and vascular endothelial growth factor (VEGF) mRNA levels in adipose-derived stem cells. Norepinephrine further increased VEGF mRNA expression under hypoxia; this effect was abolished by doxazosin.

[Scientific Reports] The contribution of select matrix metalloproteinases (MMPs) and tissue inhibitors (TIMPs) to the progression of myocardial infarction and progressive sudden death was examined in Apoe-deficient mice with concomitant deletion of Mmp7, Mmp9, Mmp12, or Timp1 and relevant wild-type controls after 36-weeks high-fat feeding.

[Stem Cell Research & Therapy] The authors investigated whether sevoflurane preconditioning could promote MSCs to attenuate myocardial I/R injury via transient receptor potential canonical channel 6 (TRPC6)-induced angiogenesis.