Publications by authors named "B Demeulder"
Article Synopsis
- - The study investigates whether high blood eosinophil counts have the same clinical significance in COPD (Chronic Obstructive Pulmonary Disease) as they do in asthma, revealing ongoing debates in the medical community.
- - Researchers analyzed data from two cohorts (COPD and asthma) to study gene expression and the relationship between eosinophil counts and clinical characteristics, finding distinct genetic responses between the two conditions.
- - The findings indicate that while asthma and COPD may share some clinical features, their underlying molecular mechanisms differ significantly, emphasizing the complexity of treating these respiratory diseases.
AMP-activated protein kinase (AMPK) has been shown to inhibit cardiac hypertrophy. Here, we show that submaximal AMPK activation blocks cardiomyocyte hypertrophy without affecting downstream targets previously suggested to be involved, such as p70 ribosomal S6 protein kinase, calcineurin/nuclear factor of activated T cells (NFAT) and extracellular signal-regulated kinases. Instead, cardiomyocyte hypertrophy is accompanied by increased protein O-GlcNAcylation, which is reversed by AMPK activation.
View Article and Find Full Text PDFThis study was designed to better understand the molecular mechanisms involved in the anabolic resistance observed in elderly people. Nine young (22 ± 0.1 years) and 10 older (69 ± 1.
View Article and Find Full Text PDFEndoplasmic reticulum (ER) stress is a central actor in the physiopathology of insulin resistance (IR) in various tissues. The subsequent unfolded protein response (UPR) interacts with insulin signaling through inositol-requiring 1α (IRE1α) activation and tribbles homolog 3 (TRB3) expressions. IRE1α impairs insulin actions through the activation of c-Jun N-terminal kinase (JNK), and TRB3 is a pseudokinase inhibiting Akt.
View Article and Find Full Text PDFEukaryotic elongation factor 2 (eEF-2) and mammalian target of rapamycin (mTOR)-p70 ribosomal protein S6 kinase (p70S6K) signaling pathways control protein synthesis and are inhibited during myocardial ischemia. Intracellular acidosis and AMP-activated protein kinase (AMPK) activation, both occurring during ischemia, have been proposed to participate in this inhibition. We evaluated the contribution of AMPKα2, the main cardiac AMPK catalytic subunit isoform, in eEF2 and mTOR-p70S6K regulation using AMPKα2 KO mice.
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