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CaMKIIγ advances chronic intermittent hypoxia-induced cardiomyocyte apoptosis via HIF-1 signaling pathway.
Sleep Breath
January 2025
Nantong Key Laboratory of Translational Medicine in Cardiothoracic Diseases, and Research Institution of Translational Medicine in Cardiothoracic Diseases, Affiliated Hospital of Nantong University, Nantong, Jiangsu, 226001, China.
Background: Our previous study have demonstrated chronic intermittent hypoxia (CIH) induced cardiomyocyte apoptosis and cardiac dysfunction. However, the molecular mechanisms are complicated and varied. In this study, we first investigated the CaMKIIγ expression and signaling pathway in the pathogenesis of cardiomyocyte apoptosis after CIH.
View Article and Find Full Text PDFSignalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.
PLoS One
January 2025
Department of Cardiovascular Sciences, Anaesthesia, Critical Care and Pain Management, University of Leicester, Leicester, United Kingdom.
Sustained pathologic myocardial hypertrophy can result in heart failure(HF); a significant health issue affecting a large section of the population worldwide. In HF there is a marked elevation in circulating levels of the peptide urotensin II(UII) but it is unclear whether this is a result of hypertrophy or whether the high levels contribute to the development of hypertrophy. The aim of this study is to investigate a role of UII and its receptor UT in the development of cardiac hypertrophy and the signalling molecules involved.
View Article and Find Full Text PDFCalcium/calmodulin-dependent protein kinase II α and β differentially regulate mammalian sleep.
Commun Biol
January 2025
Chinese Institute of Brain Research, Beijing (CIBR), and Chinese Institutes for Medical Research, Beijing (CIMR), Capital Medical University, Beijing, China.
While sleep is important, our understanding of its molecular mechanisms is limited. Over the last two decades, protein kinases including Ca/calmodulin-dependent protein kinase II (CaMKII) α and β have been implicated in sleep regulation. Of all the known mouse genetic mutants, the biggest changes in sleep is reported to be observed in adult mice with sgRNAs for Camk2b injected into their embryos: sleep is reduced by approximately 120 min (mins) over 24 h (hrs).
View Article and Find Full Text PDFAberrant extracellular dopamine clearance in the prefrontal cortex exhibits ADHD-like behavior in NCX3 heterozygous mice.
FEBS J
January 2025
Research Center for Pharmaceutical Development, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Article Synopsis
- ADHD is linked to dopaminergic dysfunction in the prefrontal cortex, leading to symptoms like hyperactivity, inattention, and cognitive deficits.
- Researchers identified sodium-calcium exchanger 3 (NCX3) in dopaminergic neurons, finding that its knockdown causes abnormal dopamine influx and related behavioral issues in mice.
- NCX3 heterozygous mice display ADHD-like behaviors, such as hyperactivity and cognitive deficits, which can be improved with methylphenidate, highlighting the role of NCX3 in dopamine signaling and ADHD.
CaMKII-dependent non-canonical RIG-I pathway promotes influenza virus propagation in the acute-phase of infection.
mBio
January 2025
Department of Molecular Life Sciences, Graduate School of Life and Medical Sciences, Doshisha University, Kyotanabe, Japan.
Ca/calmodulin-dependent protein kinase II (CaMKII) is one of hundreds of host-cell factors involved in the propagation of type A influenza virus (IAV), although its mechanism of action is unknown. Here, we identified CaMKII inhibitory peptide M3 by targeting its kinase domain using affinity-based screening of a tailored random peptide library. M3 inhibited IAV cytopathicity and propagation in cells by specifically inhibiting the acute-phase activation of retinoic acid-inducible gene I (RIG-I), which is uniquely regulated by CaMKII.
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