Calmodulin kinase II inhibition suppresses atrioventricular conduction by regulating intracellular Ca homeostasis.

Background: Ca/calmodulin-dependent protein kinase II (CaMKII) inhibition decelerates atrioventricular node (AVN) conduction, providing a potential treatment of tachycardia. However, the effectiveness of CaMKII inhibition on tachycardia and its underlying mechanism remains unclear.

Objective: We aimed to assess the effectiveness of CaMKII inhibition in reducing ventricular rates during atrial fibrillation and to elucidate the underlying mechanism in affecting AVN electrophysiology.

MFG-E8 facilitates heart repair through M1/M2 polarization after myocardial infarction by inhibiting CaMKII.

Background: M1/M2 macrophage polarization affects patient outcomes after myocardial infarction (MI). The relationship between milk fat globule-epidermal growth factor 8 (MFG-E8) and Ca/calmodulin-dependent protein kinase II (CaMKII) on macrophage polarization after MI is unknown. To investigate the functional role of MFG-E8 in modulating cardiac M1/M2 macrophage polarization after MI, especially its influence on CaMKII signaling.

Case report: A rare case of left ventricular noncompaction in two Chinese siblings with becker muscular dystrophy caused by deletion of exons 10 to 12 in the gene.

Background: Becker muscular dystrophy (BMD) is an inherited X-linked recessive condition resulting from mutations of the gene encoding dystrophin. Left ventricular noncompaction (LVNC) is a rare cardiomyopathy morphologically characterized by abnormal myocardial trabeculae and deep recesses in the left ventricle. LVNC in BMD patients has only rarely been reported.

Pathological implication of CaMKII in NF-κB pathway and SASP during cardiomyocytes senescence.

Senescence-associated secretory phenotype (SASP) could be developed during heart ageing. But the role of SASP in cardiomyocytes senescence and its molecular mechanism remains undetermined. In this study, we observed elevated Ca/calmodulin -dependent protein kinase II (CaMKII) activation in both physiological aged heart and premature senescent cardiomyocytes.

CaMKII inhibition protects against hyperthyroid arrhythmias and adverse myocardial remodeling.

Hyperthyroidism can potentiate arrhythmias and cardiac hypertrophy, whereas Ca/calmodulin-dependent kinase II (CaMKII) promotes maladaptive myocardial remodeling. However, it remains unclear whether CaMKII contributes to the progression of hyperthyroid heart disease (HHD). This study demonstrated that CaMKII inhibition can relieve adverse myocardial remodeling and reduce sinus tachycardia, isoproterenol-induced atrial fibrillation, and ventricular arrhythmias in hyperthyroid mice with preserved heart function.

Ca/calmodulin-dependent protein kinase II inhibition reduces myocardial fatty acid uptake and oxidation after myocardial infarction.

An AMP-activated kinase (AMPK) signaling pathway is activated during myocardial ischemia and promotes cardiac fatty acid (FA) uptake and oxidation. Similarly, the multifunctional Ca/calmodulin-dependent protein kinase II (CaMKII) is also triggered by myocardial ischemia, but its function in FA metabolism remains unclear. Here, we explored the role of CaMKII in FA metabolism during myocardial ischemia by investigating the effects of cardiac CaMKII on AMPK-acetyl-CoA carboxylase (ACC), malonyl CoA decarboxylase (MCD), and FA translocase cluster of differentiation 36 (FAT/CD36), as well as cardiac FA uptake and oxidation.

Maternal vitamin D intake during pregnancy and risk of asthma and wheeze in children: a systematic review and meta-analysis of observational studies.

To summarize the relationship between vitamin D and infant asthma or wheeze. We used PubMed and Embase to search articles through July 2017 with selection criteria for relevant studies. Random-effect models were used to pool the results of included studies.

Sleep duration and risk of coronary heart disease: A systematic review and meta-analysis of prospective cohort studies.

Background: Epidemiological studies suggest an association between sleep duration and risk of coronary heart disease, however, the results are controversial. We conducted this systematic review and meta-analysis to summarize the potential dose-response relationship between sleep duration and risk of coronary heart disease.

Methods: The electronic reference databases (PubMed and Embase) were searched through January 2016 with selection criteria for relevant studies.

Relaxin-2 improves diastolic function of pressure-overloaded rats via phospholamban by activating Akt.

Background: Relaxin is a peptide hormone which has been demonstrated to be safe and has a therapeutic effect on acute heart failure in clinic trials. However, its effect on diastolic function is still unknown. The aims of the study were to determine whether relaxin could improve the diastolic function in pressure-overloaded rat model and to analyze potential mechanisms.

Elevated soluble ST2 and depression increased the risk of all-cause mortality and hospitalization in patients with heart failure.

This study aimed to assess the predictive effect of soluble ST2 (sST2) and depressive symptoms in patients with heart failure (HF) and to determine whether the prognosis of HF patients with preserved ejection fraction (HFpEF) differs from those with reduced ejection fraction (HFrEF). A cohort of 233 HF patients was followed for 1 year. Depressive symptoms were evaluated by the Hospital Anxiety and Depression Scale.