Hypertrophy of myocardium, developed within 4 weeks after aorta stenosis, led to alteration in content of adrenaline in heart tissue as well as in some pathways of cAMP turnover: decrease in content of cAMP, an increase in the basal activity of adenylate cyclase, decrease in activation of the enzyme by adrenaline; activity of phosphodiesterase was not distinctly altered. Under conditions of hyperbaric oxygenation hypertrophy of myocardium became less distinct, content of cAMP was increased up to the normal value, the increased basal activity of adenylate cyclase was slightly decreased, whereas sensitivity of the enzyme to adrenaline did not reduce, content of adrenaline was increased.
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Circ Res
January 2025
Key Laboratory of Drug Targets and Translational Medicine for Cardio-cerebrovascular Diseases, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Jiangsu, China (X.T., X.L., X.S., Y. Zhang, Y. Zu, Q.F., L.H., S.S., F.C., L.X., Y.J.).
Background: The decrease in S-nitrosoglutathione reductase (GSNOR) leads to an elevation of S-nitrosylation, thereby exacerbating the progression of cardiomyopathy in response to hemodynamic stress. However, the mechanisms under GSNOR decrease remain unclear. Here, we identify NEDD4 (neuronal precursor cell expressed developmentally downregulated 4) as a novel molecule that plays a crucial role in the pathogenesis of pressure overload-induced cardiac hypertrophy, by modulating GSNOR levels, thereby demonstrating significant therapeutic potential.
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January 2025
Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Protein homeostasis is crucial for maintaining cardiomyocyte (CM) function. Disruption of proteostasis results in accumulation of protein aggregates causing cardiac pathologies such as hypertrophy, dilated cardiomyopathy (DCM), and heart failure. Here, we identify ubiquitin-specific peptidase 5 (USP5) as a critical determinant of protein quality control (PQC) in CM.
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January 2025
Physiologisches Institut, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.
NO-sensitive guanylyl cyclase (NO-GC) is involved in the (patho)physiology of the mammalian heart. However, little is known about the individual cardiac cell types that express NO-GC and the role of the enzyme in cardiac fibrosis. Here, we describe the cellular expression of NO-GC in healthy and fibrotic murine myocardium; these data were compared with scRNA-seq data.
View Article and Find Full Text PDFJ Anat
January 2025
Hannover Medical School, Institute of Functional and Applied Anatomy, Hannover, Germany.
Obesity, along with hypoxia, is known to be a risk factor for pulmonary hypertension (PH), which can lead to right ventricular hypertrophy and eventually heart failure. Both obesity and PH influence the autonomic nervous system (ANS), potentially aggravating changes in the right ventricle (RV). This study investigates the combined effects of obesity and hypoxia on the autonomic innervation of the RV in a mouse model.
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January 2025
Department of Physiology, Zunyi Medical University, Campus No.1 Road, Xinpu New District, Zunyi, 563006, Guizhou, China.
In the vascular system, angiotensin II (Ang II) mediated vasoconstriction by inducing the production of 20-hydroxyeicosatetraenoic acid (20-HETE). However, the role of 20-HETE in Ang II-induced cardiac dysfunction had yet to be fully elucidated. This study investigated the effects of Ang II on CYP4A expression and 20-HETE production in H9c2 cells using RT-qPCR, Western blot, and ELISA.
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