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Cardiac Hypertrophy - Crossref

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Last Updated: 10 September 2022

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Cardiomyocyte BRAF is a key signalling intermediate in cardiac hypertrophy in mice

Here, we used mice with a tamoxifen-inducible cardiomyocyte-specific BRAF knockout to see the role of BRAF in hypertension-associated cardiac hypertrophy caused by angiotensin II and physiological hypertrophy induced by phenylephrine. In mice with CM-BRAFKO, cardiomyocyte hypertrophy and increased fibrosis were restricted within the myocardium and around the arterioles in male mice; cardiomyocyte hypertrophy and increased fibrosis; cardiomyocyte hypertrophy and increased fibrosis were restricted; cardiomyocyte hypertrophy and interstitial fibrosis were inhibited; cardiomyocyte hypertrophy and increased fibrosis. Phenylephrine had limited effect on fibrosis, but it promoted cardiomyocyte hypertrophy and increased contractility in male mice; cardiomyocyte hypertrophy was unaffected in mice with CM-BRAFKO mice, but contractility was unaffected in mice with CM-BRAFKO mice, but the rise in contractility was reduced and fibrosis increased. Female mice had a modest hypertrophic response, and Phenylephrine-induced cardiomyocyte BRAF decreased cardiomyocyte size, but had no effect on fibrosis and increased contractility in male mice, as opposed to males.

Source link: https://doi.org/10.1101/2022.09.07.506723


Control of Pathological Cardiac Hypertrophy by Transcriptional Corepressor IRF2BP2 (Interferon Regulatory Factor-2 Binding Protein 2)

However, how the transcriptional activity of NFAT1 in terms of cardiac hypertrophy is controlled at the transcriptional level has not been well understood. Our in vitro experiments revealed that although IRF2BP2 loss-of-function exacerbation-induced cardiac hypertrophic response was exacerbated by cardiomyocyte-specific Irf2bp2 knockout and Irf2bp2 –transgenic mouse strains, Irf2bp2 -transgenic mouse strains led to both aortic banding- and angiotensin II infusion-induced cardiac hypertrophic response, Irf2BP2 exacerbatedoutput: Irf2BP2BP2BP2bp2 exacerbated myrf2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2bp2b2bvy and anady inflammatory response, and anabp2bp2bp2bp2b2bp As a result, the devastating effect of Irf2bp2 deficiency on cardiac hypertrophy was largely reversed by NFAT1 blockage.

Source link: https://doi.org/10.1161/hypertensionaha.116.08728


Abstract P123: Angiotensin Ii Type 1a Receptor Expressed Insmooth Muscle Cells Is Required Forangiotensin Ii-induced Vascular Remodeling But Not For Cardiac Hypertrophy

Angiotensin II Type 1a Receptor has been shown to play a vital role in cardiovascular disease. We have shown that ADAM17 mediates cardiovascular remodeling induced by angiotensin II by using a SM22 u03b1 Cre reporter, which indicates SM22-u03b1 Cre reporter, which indicates changes in smooth muscle cells and cardiomyocytes. However, we have limited information about how SMC AT1a receptors influence vascular fibrosis and cardiac hypertrophy. Using two distinct SMC AT1a receptor deficient mice, this research was intended to clarify the role of the SMC AT1a receptor in cardiovascular remodeling. Both KISMKO and SMMHCKO mice's perivascular fibrosis in coronary arteries was elevated in control mice and attenuated in both KISMKO and SMMHCKO mice, according to a Histological study. In both KISMKO and SMMHCKO mice, the descending aorta was increased in control mice, but these phenotypic changes were attenuated.

Source link: https://doi.org/10.1161/hyp.79.suppl_1.p123


Abstract P120: Left Ventricular Hypertrophy Is Associated With Higher Cardiac Biomarkers In Patients With Covid-19

Introduction: Left ventricular hypertrophy is a risk factor for cardiovascular disease such as heart arrest and arrhythmia. LVH rises left ventricular mass with myocardial fibrosis, which may lead to COVID-19-induced cardiac dysfunction. Hypothesis: LVH is a predictor of poor outcomes in patients with COVID-19. Methods: We conducted a two-center retrospective review of 415 adult patients hospitalized with COVID-19 from March 2020 to September 2021 who had an echocardiogram performed while inpatient. In the LVH group, NT-proBNP and peak troponin I levels were both elevated. Conclusion: LVH was remarkably associated with other cardiovascular risk factors and elevated cardiac biomarkers, indicating a greater risk of cardiac disease in LVH patients with COVID-19. To determine whether LVH is an accurate predictor of COVID-19-induced cardiac disease, studies with a larger sample size are needed.

Source link: https://doi.org/10.1161/hyp.79.suppl_1.p120


Abstract 068: Genetic Mechanisms Of Cardiac Hypertrophy And Fibrosis In Global Npr1 Gene-ablated Male And Female Mice

The goal of this research was to determine the factors controlling cardiac hypertrophy and fibrosis in global Npr1 gene-knockout mice, and whether transforming growth factor-beta 1 plays a vital role in this process. Both male and female Npr1 KO, heterozygous, and wild-type mice were treated with TGF-u203b21 receptor antagonist GW788388 by intraperitoneal injection for 28 days. In Npr1 KO mice, the HW/BW and TL/BW ratios were noticeably higher in males and females, and significantly higher in males than females. Compared to WT mice, Npr1 -/- mice showed significant increases in cardiac hypertrophic marker collagen-13b1 and fibrotic markers, monocyte chemoattractant protein, connective tissue growth factor, and alpha-smooth muscle actin. In male KO mice than female KO mice, the left ventricular end-systolic and diastolic dimensions as well as posterior wall thickness were noticeably higher than in female KO mice than female KO mice compared to WT mice. Male KO mice were faster at shortening than female KO mice, but female KO mice were not affected.

Source link: https://doi.org/10.1161/hyp.79.suppl_1.068


Abstract P095: Arginine Vasopressin Infusion Is Sufficient To Cause Pregnancy-specific Cardiac Hypertrophy

In mice, arginine vasopressin infusion resurrects medical signs of PE, including pregnancy-specific hypertension, according to previous published reports. We hypothesized that prolonged AVP infusion in pregnant mice would cause cardiac hypertrophy. For a case control investigation, Human 3rd trimester maternal plasma samples were obtained from the Iowa Maternal Fetal Tissue Bank. In plasma samples from pre-eclamptic patients, there was a significant 264. 6 pg/ml rise in NT-ProBNP and MR-proANP respectively, as compared to normal pregnancy plasma, with a 27. 9% u00b1 11. 5 pg/ml rise. A 6. 6 and 1. 8 fold rise in rat ANP and BNP expression were observed respectively in rat cardiomyocytes treated with pooled plasma from preeclamptic patients. These findings indicate that AVP infusion in mice specifically during pregnancy is sufficient to cause cardiac hypertrophy similar to that seen in a normal pregnancy, and that unknown circulating factors in preeclamptics may play a role in hypertrophy.

Source link: https://doi.org/10.1161/hyp.79.suppl_1.p095


Nocturia independently predicts left ventricular hypertrophy and left atrial enlargement among patients with cardiac symptoms

Abstract: Urological disorders and systemic diseases, as well as heart disease, can cause nocturia. On echocardiography, we wanted to investigate the connection between nocturia and structural abnormalities. Adult patients with cardiac signs or heart murmur, as well as a history of structural heart disease were eligible. Patients aged u2265-65 years, hypertension, and left atrial enlargement were two of the common causes of more frequent episodes of bothersome nocturia. In addition, bothersome nocturia can predict both LAE and left ventricular hypertrophy in the elderly. Patients with persistent nocturia with no other significant lower urinary tract signs should be referred to cardiologists.

Source link: https://doi.org/10.1038/s41598-022-19190-9


Ca2+/Calmodulin-Dependent Protein Kinase II Regulation by Inhibitor of RIPK3 Protects against Cardiac Hypertrophy

cardiovascular disease is a result of coronary disease's mechanisms. Ca2+/calmodulin-dependent protein kinase II u03b4's function is crucial to cardiovascular disease mechanisms. u03b4's function is key to cardiovascular disease pathogenesis. The present study is intended to find out how the RIPK3 inhibitor GSKu2019872 restricts CaMKII production and investigates the effect on hypertrophic cardiomyopathy. After WT mice were induced by AngII for 72 hours, they were given GSKu2019872 with an intraperitoneal dose of 6 mg/kg every two weeks, twice a day for two weeks. GSKu2019872 deletion of the RIPK3 gene or administration thereof may inhibit CaMKII activity, relieve oxidative stress, minimize necroptosis, and restore myocardial injury and cardiac dysfunction caused by AngiI-induced cardiac hypertrophy in mice. CaMKII activation and necroptosis contribute to cardiac hypertrophy in a RIPK3-dependent fashion, which may lead to therapeutic options for HCM. The present study found that CaMKII activation and necroptosis exacerbate cardiac hypertrophy in a RIPK3-dependent fashion, which may include therapeutic strategies for HCM. GSK3 inhibitor GSKu2019872 has a protective effect on cardiac hypertrophy, and it may be an affordable targeted medicine for HCM in clinical therapy.

Source link: https://doi.org/10.1155/2022/7941374


Genetic Architecture of Heart Mitochondrial Proteome influencing Cardiac Hypertrophy

Utilizing an integrative proteomics approach in a panel of inbred mouse strains called the Hybrid Mouse Diversity Panel, we present an investigation of common genetic variations contributing to mitochondrial and heart functions. In two independent heart stress models, namely, isoproterenol-induced heart failure and diet-induced obesity models, the three were correlated with heart mass. We developed co-expression protein networks using weighted gene co-expression network analysis to determine the aspects of mitochondrial metabolism regulated by these loci. These results show that common variants of certain mitochondrial proteins can influence mitochondrial functions and heart hypertrophy and contribute to heart hypertrophy, as well as other human genetic susceptibility to heart disease in human populations.

Source link: https://doi.org/10.1101/2022.08.24.505177


Protections of transcription factor BACH2 and natural product myricetin against pathological cardiac hypertrophy and dysfunction

Heart failure can be caused by a pathological hypertrophic myocardium under persistent adverse conditions. To knock down Bach2, nenatal rat ventricular myocytes were isolated and infected with lentivirus to overexpress Bach2 or transfected with siRNA to knock down Bach2. Our results revealed that overexpression of BACH2 improved TAC-induced cardiac hypertrophy and failure in mice and mice, as well as decreased isoproterenol-triggered myocyte hypertrophy in NRVMs. BACH2 bound to the promotor region of Akap6 at the -600 to -587 location and repressed its expression, serving as a vital scaffold for cardiac hypertrophy and failure signaling pathways, according to further assays. Based on a small molecular natural product library review, myricetin may up-regulate expression of Bach2 and simultaneously reduce the transcriptional levels of hypertrophic marker genes Bnp and Myh7. Myricetin was shown to have a BACH2-dependent protective role against cardiac hypertrophy in vivo and in vitro, according to further research.

Source link: https://doi.org/10.3389/fphys.2022.971424

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions