Previous evidences suggested that atorvastatin not only reduced blood lipids but also reduced myocardial hypertrophy and remodeling. And it was reported that C/EBPβ (CCAAT/enhancer-binding protein β) played a pivotal role both in the physiologic and pathological cardiac hypertrophy. However, it has not been reported before whether this signaling pathway of C/EBPβ participates in protective effect of atorvastatin for hypertrophy cardiomyocytes. In present study, We found that overexpression of C/EBPβ significantly abrogated the effect of atorvastatin on increasing Bcl-2/Bax and PGC-1α while the early and late apoptosis rate increased and mitochondrial membrane potential (MMP) was reduced. In conclusion, we further identified the protective effect of atorvastatin on hypertrophic cardiomyocytes induced by Angiotensin II by rescuing the MMP and inhibiting apoptosis, which might be at least partly attributed to down-regulation of C/EBPβ. And C/EBPβ might be a new target to rescue mitochondrion function and apoptosis in pathological cardiac hypertrophy.
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http://dx.doi.org/10.1016/j.bbrc.2017.03.057 | DOI Listing |
Sci 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 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.
View Article and Find Full Text PDFSci Rep
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.
View Article and Find Full Text PDFCell Biochem Biophys
January 2025
Department of Pharmacy, The Fourth Affiliated Hospital of Soochow University, Jiangsu, Suzhou, 215000, China.
Total glucosides of paeony (TGP) have been investigated for their effects on cardiomyocyte hypertrophy induced by angiotensin II (Ang II). In this study, rat cardiomyocyte H9c2 cells were treated with various doses of TGP (0, 12.5, 25, 50, 100, 200, and 400 μmol/L), and cell viability was assessed using the MTT method to determine an optimal dose.
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