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Cardiac hypertrophy is necessary for the heart to cope with an increase in workload. BRAF was involved in hypertension-associated cardiac hypertrophy caused by angiotensin II and physiological hypertrophy induced by phenylephrine in mice with tamoxifen-inducible cardiomyocyte-specific BRAF knockout here in this review. In mice with CM-BRAFKO, cardiomyocyte hypertrophy and increased fibrosis within myocardium and around the arterioles; cardiomyocyte hypertrophy and increased fibrosis were inhibited; cardiomyocyte hypertrophy and increased fibrosis were inhibited in mice with AngII; cardiomyocyte hypertrophy and increased fibrosis. Phenylephrine had a limited effect on fibrosis, but it promoted cardiomyocyte hypertrophy and increased contractility in male mice, but cardiomyocyte hypertrophy was unaffected in mice with CM-BRAFKO mice, but the increase in contractility was minimized and fibrosis accelerated. In female mice, Phenylephrine triggered a modest hypertrophic response, and, in comparison to males, tamoxifen-induced decrease in cardiomyocyte BRAF reduced cardiomyocyte size, causing no effect on fibrosis and increased contractility.
Source link: https://europepmc.org/article/PPR/PPR541269
Background Cardiac hypertrophy is first an adaptive response of cardiomyocytes to neurohumoral or hemodynamic stimuli. Evidence reveals that Ang II or pressure overload causes GSDMD synthesis in cardiomyocytes and myocardial tissues. Methods and findings In this research, we investigated the aberrant activation of GSDMD in mouse and human hypertrophic myocardia, and mice's cardiomyocyte pyroptosis, which was related to GSDMD deficiency. In addition, deficiency of both GSDMD and STING inhibited cardiac hypertrophy in cardiac-specific GSDMD-overexpressing mice.
Source link: https://europepmc.org/article/MED/36065823
However, the mechanisms by which Res relieves cardiac hypertrophy have yet to be fully explained. To determine the effect of Res on cardiac hypertrophy, network pharmacology was used to establish a network and perform enrichment analysis in the current research. Experimental validation was conducted using 40 Sprague u2011Dawley rats administered intragastric 80 mg/day Res and 20 mg/kg/day for 4 weeks. Res's anti-cardiac hypertrophy effects were significantly reduced by autophagy inhibitor 3u2011MA.
Source link: https://europepmc.org/article/MED/36052855
By degrading cAMP and cGMP, Cyclic nucleotide phosphodiesterases modulate cardiac function's neurohormonal regulation of cardiac function. Local pools of cyclic nucleotides and specific functions are controlled in cardiomyocytes by multiple PDE isozymes with different enzymatic properties and subcellular localization. In this Essay, we explore cAMP and cGMP signalling in cardiomyocytes and show the various PDE families expressed in the heart, as well as their changes in pathological cardiac hypertrophy and HF. In addition, we also analyze the results from preclinical studies as well as clinical studies pointing to the use of inhibitors or activators of specific PDEs that may have therapeutic value in HF.
Source link: https://europepmc.org/article/MED/36050457
Nocturia can be related to urological disorders and systemic diseases, including heart disease. On echocardiography, we wanted to investigate the relationship between nocturia and morphological abnormalities. Adult patients with heart murmur, or a history of structural heart disease were included in an echocardiography study. Patients aged u2265-60 years, hypertension, and left atrial enlargement were associated with higher incidences of bothersome nocturia in patients aged 65 to 65. In addition, bothersome nocturia could be the source of both LAE and left ventricular hypertrophy in elderly patients. Patients with persistent nocturia without some other significant urinary tract disorders should be referred to cardiologists.
Source link: https://europepmc.org/article/MED/36050443
Abstract The relationship between mitochondrial function and pathological myocardial hypertrophy is shown by a nonselective cation channel that mediates the association between mitochondrial function and pathological myocardial hypertrophy. After pressure overload-induced myocardial hypertrophy, this research sought to determine whether TRPV1 stimulation improves the morphology and function of intracellular mitochondria to shield cardiomyocytes. In addition, TRPV1 reduces cardiomyocyte area and improves mitochondrial function by encouraging mitochondria-associated endoplasmic membrane formation in a phenylephrine-treated cardiomyocyte hypertrophy model, which was demonstrated in vitro experiments. Activation of TRPV1 reduced mitochondrial reactive oxygen species caused by phenylephrine, according to TRPV1, whereas siMFN2 disruption destroyed mitochondrial shields, resulting in mitochondrial shielding. TRPV1's findings show that TRPV1 helps reduce pressure overload-induced cardiac hypertrophy by increasing MAM formation and saved mitochondrial function in cardiomyocytes by the AMP-activated protein kinase/MFN2 pathway.
Source link: https://europepmc.org/article/MED/35881904
We created 3--7-hydroxy-2H-chromen-2-one, a novel SIRT3 activator, in this study, by structural optimization of the first SIRT3 agonist C12. The value of 23. 2 u00b5M is the product of a 5 million dollars. We demonstrated that SZC-6 was directly bound to SIRT3 with a KD value of 15 bcM, a J d value of 15 mm; cm; and that SIRT3 deacetylation rate has increased with EC 50 value of 23. 2 u00b5M. In wild-type mice, ISO treatment dose-dependently reversed ISO-induced diastolic and systolic cardiac function, but not in SIRT3 knockdown mice. SiRT3 activation by SZC-6 increased ATP production and rate of mitochondrial oxygen consumption, as well as reduced ROS, as well as reduced ROS, boosting mitochondrial function in ISO-treated NRCMs. SZC-6 dose-dependently elevated LKB1 phosphorylation in the LKB1 region, thus promoting AMPK activation to reduce Drp1-dependent mitochondrial fragmentation.
Source link: https://europepmc.org/article/MED/36042291
Although the role of p53 and p21 in pathological cardiac hypertrophy has been investigated, the relationship between them in cardiomyocytes is also unknown. We found that both p53 and p21 expression in neonatal rat ventricular myocytes were modulated by specific adenoviruses and siRNAs, and they both promoted each other's expression, as well as increasing p53 and p21 expression in neonatal rat ventricular myocytes' expression.
Source link: https://europepmc.org/article/MED/36044972
Hyperthyroidism-induced cardiac hypertrophy in a rat model of hyperthyroidism-induced cardiac hypertrophy was investigated by the present study. Rats from four separate groups were randomly assigned: control, cardiac hypertrophy, CH + valsartan, and CH + LCZ696. Compared to CH group rats, LCZ696 or valsartan significantly improved hemodynamic abnormalities, normalized serum natriuretic peptide, fibroblast growth factor-23, and cardiac inflammatory markers. PPAR-u03d2, mir-377, and let-7b were tested in clinical expression profiles of autophagy markers, fibrotic markers, LCZ696 or valsartan, as well as let-7B.
Source link: https://europepmc.org/article/MED/36030321
Using an integrative proteomics approach in a panel of inbred mouse strains called the Hybrid Mouse Diversity Panel, we present an analysis of common genetic variations that influence mitochondrial and heart functions. In two independent heart stress models, namely, isoproterenol-induced heart failure and diet-induced obesity models, variations of all three were linked with heart mass, including heart failure and diet-induced obesity models. We established co-expression protein networks to determine the aspects of mitochondrial metabolism controlled by these loci's regulation, as shown by these loci. These findings show that common variants of certain mitochondrial proteins can influence mitochondrial function and contribute to heart hypertrophy and heart hypertrophy, as well as heart hypertrophy.
Source link: https://europepmc.org/article/PPR/PPR537231
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