In rabbits, arterial hypertension was simulated according to Goldblatt. One, 2, 4, and 6 weeks after surgery, the hearts of control and experimental animals were extirpated for morphological examination. In semithin sections of the left and right ventricles, morphometry was performed using an Avtandilov grid. Ultrathin sections of these organs were examined under an electron microscope. It was found that the initial signs of myocardial hypertrophy appeared soon after hypertension modeling, and more early in the right ventricle. Activation of apoptosis was noted in cardiomyocytes of both ventricles, and its intensity correlated with the degree of myocardial hypertrophy. It is hypothesized that apoptosis limits the development of hypertrophy in the myocardium.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1023/b:bebm.0000031552.11912.a1 | DOI Listing |
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.
View Article and Find Full Text PDFJ Magn Reson Imaging
January 2025
Department of Cardiology, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Background: Hemodynamic force (HDF) from cardiac MRI can indicate subclinical myocardial dysfunction, and help identify early cardiac changes in patients with Fabry disease (FD). The hemodynamic change in FD patients remains unclear.
Purpose: To explore HDF changes in FD and the potential of HDF measurements as diagnostic markers indicating early cardiac changes in FD.
J Physiol Sci
January 2025
Experimental Physiology and Biochemistry Laboratory. Physical Education and Sport Center, Federal University of Espirito Santo, Vitoria, Brazil. Electronic address:
Background/objectives: Myocardial infarction (MI) frequently leads to cardiac remodeling and failure with impaired life quality, playing an important role in cardiovascular deaths. Although physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases, the effects of strength training (ST) on the structural and functional aspects of cardiac remodeling need to be further documented. In this study, we aimed to investigate the role of a linear block ST protocol in the rat model of MI.
View Article and Find Full Text PDFSci Adv
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.
View Article and Find Full Text PDFiScience
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 PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!