NPS-2143 inhibit glioma progression by suppressing autophagy through mediating AKT-mTOR pathway.

Gliomas are the most common tumours in the central nervous system. In the present study, we aimed to find a promising anti-glioma compound and investigate the underlying molecular mechanism. Glioma cells were subjected to the 50 candidate compounds at a final concentration of 10 μM for 72 h, and CCK-8 was used to evaluate their cytotoxicity.

Carbon doped hexagonal boron nitride as an efficient metal-free catalyst for NO capture and reduction.

The electrochemical NO reduction reaction (NORR) towards NH is considered a promising strategy to cope with both NO removal and NH production. Currently, the research on NORR electrocatalysts mainly focuses on metal-based catalysts, while metal-free catalysts are quite scarce. In this work, we have systematically investigated the properties of pristine and C/O doped h-BN for efficient NO capture and reduction.

Obesity and atrial fibrillation: a narrative review from arrhythmogenic mechanisms to clinical significance.

The prevalence of obesity and atrial fibrillation (AF), which are inextricably linked, is rapidly increasing worldwide. Obesity rates are higher among patients with AF than healthy individuals. Some epidemiological data indicated that obese patients were more likely to develop AF, but others reported no significant correlation.

Homology-directed repair of an MYBPC3 gene mutation in a rat model of hypertrophic cardiomyopathy.

Variants in myosin-binding protein C3 (MYBPC3) gene are a main cause of hypertrophic cardiomyopathy (HCM), accounting for 30% to 40% of the total number of HCM mutations. Gene editing represents a potential permanent cure for HCM. The aim of this study was to investigate whether genome editing of MYBPC3 using the CRISPR/Cas9 system in vivo could rescue the phenotype of rats with HCM.

Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors.

Cardiac hypertrophy is a key process in cardiac remodeling development, leading to ventricle enlargement and heart failure. Recently, studies show the complicated relation between cardiac hypertrophy and epigenetic modification. Post-translational modification of histone is an essential part of epigenetic modification, which is relevant to multiple cardiac diseases, especially in cardiac hypertrophy.

Epigenetic Mechanism and Therapeutic Implications of Atrial Fibrillation.

Atrial fibrillation (AF) is the most common arrhythmia attacking 1. 5-2.0% of general population worldwide.

Genetic inhibition of nuclear factor of activated T-cell c2 prevents atrial fibrillation in CREM transgenic mice.

Aims: Abnormal intracellular calcium (Ca2+) handling contributes to the progressive nature of atrial fibrillation (AF), the most common sustained cardiac arrhythmia. Evidence in mouse models suggests that activation of the nuclear factor of activated T-cell (NFAT) signalling pathway contributes to atrial remodelling. Our aim was to determine the role of NFATc2 in AF in humans and mouse models.

Trimetazidine Attenuates Heart Failure by Improving Myocardial Metabolism via AMPK.

Energic deficiency of cardiomyocytes is a dominant cause of heart failure. An antianginal agent, trimetazidine improves the myocardial energetic supply. We presumed that trimetazidine protects the cardiomyocytes from the pressure overload-induced heart failure through improving the myocardial metabolism.

The role of CD36 in cardiovascular disease.

CD36, also known as the scavenger receptor B2, is a multifunctional receptor widely expressed in various organs. CD36 plays a crucial role in the uptake of long-chain fatty acids, the main metabolic substrate in myocardial tissue. The maturation and transportation of CD36 is regulated by post-translational modifications, including phosphorylation, ubiquitination, glycosylation, and palmitoylation.

MYH7B variants cause hypertrophic cardiomyopathy by activating the CaMK-signaling pathway.

Hypertrophic cardiomyopathy (HCM) is a common genetic disease, predominantly caused by mutations in cardiac sarcomere genes; however, whether MYH7B causes HCM is not known. In this study, 549 unrelated patients with HCM and 500 healthy-controls were screened using targeted sequencing and whole exome sequencing together. We observed seven variants in MYH7B causing HCM in 8/549 patients, which accounted for 1.

Ranolazine prevents pressure overload-induced cardiac hypertrophy and heart failure by restoring aberrant Na and Ca handling.

Background: Cardiac hypertrophy and heart failure are characterized by increased late sodium current and abnormal Ca handling. Ranolazine, a selective inhibitor of the late sodium current, can reduce sodium accumulation and Ca overload. In this study, we investigated the effects of ranolazine on pressure overload-induced cardiac hypertrophy and heart failure in mice.

AMPKα2 Protects Against the Development of Heart Failure by Enhancing Mitophagy via PINK1 Phosphorylation.

Rationale: Mitochondrial dysfunction plays an important role in heart failure (HF). However, the molecular mechanisms regulating mitochondrial functions via selective mitochondrial autophagy (mitophagy) are poorly understood.

Objective: We sought to determine the role of AMPK (AMP-activated protein kinase) in selective mitophagy during HF.

P2y12 Receptor Promotes Pressure Overload-Induced Cardiac Remodeling via Platelet-Driven Inflammation in Mice.

Inflammation plays a critical role in adverse cardiac remodeling and heart failure. The P2y12 receptor is one of the predominant activating receptors for platelets, thus initiating inflammatory responses under various diseases. In this study, we investigated the functional significance of P2y12-mediated platelet activation in pressure overload-induced cardiac remodeling.

Soluble Epoxide Hydrolase Inhibition Protected against Angiotensin II-induced Adventitial Remodeling.

Epoxyeicosatrienoic acids (EETs), the metabolites of cytochrome P450 epoxygenases derived from arachidonic acid, exert important biological activities in maintaining cardiovascular homeostasis. Soluble epoxide hydrolase (sEH) hydrolyzes EETs to less biologically active dihydroxyeicosatrienoic acids. However, the effects of sEH inhibition on adventitial remodeling remain inconclusive.