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Cardiac Hypertrophy - Crossref

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Last Updated: 10 January 2023

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Left Ventricular Hypertrophy and Biomarkers of Cardiac Damage and Stress in Aortic Stenosis

Background Left ventricular hypertrophy is correlated with increased mortality risk and rehospitalization after transcatheter aortic valve replacement in those with severe aortic stenosis. It's unclear if cardiac troponinin and NT/u20ProBNP risk stratify patients with aortic stenosis and without LVH. Methods and Findings We collected 674 patients with severe aortic stenosis undergoing transcatheter aortic valve replacement in a multicenter prospective registry, with cTnT, and NTu2010proBNP, among others. All-u2010cause death rates are projected for five years, with LVH and biomarkers estimating associations, according to Cox proportional hazards models. Patients with moderate/severe LVH were found in 82% and 86% of patients with moderate/severe LVH, respectively, in comparison to 66% and 69% of patients with no/mild LVH, respectively. In a model with both biomarkers and LVH, elevated cTnT and elevated NTu2010proBNP were all associated with increased mortality risk, although severe/severe LVH was not a factor.

Source link: https://doi.org/10.1161/jaha.121.023466


A Unique High‐Output Cardiac Hypertrophy Phenotype Arising From Low Systemic Vascular Resistance in Cantu Syndrome

Background Cardiovascular hypertrophy caused by left ventricular hypertrophy is a risk factor for congestive heart disease, which is traditionally associated with reduced systolic and/or diastolic ventricular function. Left ventricular hypertrophy with enhanced ventricular function and increased cardiac output, which is potentially related to higher output heart failure and high-u2010 output heart failure, has been attributed to high output heart failure. Subjects with CS showed significant left ventricular hypertrophy and low blood pressure. With normal left ventricular wall thickness, most patients with CS displayed eccentric hypertrophy. In 4 of the 5 subjects with CS age > 40 years on long-term follow-up, heart failure symptoms were evident in four of the 5 patients. Conclusions The results reveal the natural history of high-output heart hypertrophy in subjects with CS, a key population for long-term consequences of poor systemic vascular resistance, as well as the possibility of progression to high-output heart failure in people with low output, as well as potential for progression to high-u2010 output heart failure.

Source link: https://doi.org/10.1161/jaha.122.027363


The function of LncRNA-H19 in cardiac hypertrophy

Decompensated cardiac hypertrophy is attributed to fibrosis, inflammatory cytokine, maladaptive remodeling, and heart failure. Long noncoding RNAs are noncoding RNAs that control various physiological and pathological processes by a variety of molecular mechanisms. This review provides a comprehensive summary of the latest research into the role of lncRNA-H19 in cardiac hypertrophy, including its pathophysiological pathways and underlying pathological mechanism, including calcium regulation, fibrosis, angiogenesis, inflammation, and methylation. LncRNA-H19, which is a target for cardiac hypertrophy therapy, is then discussed in the context in which it could be used to gain more insight into the potential biological functions of lncRNA-H19 in cardiac hypertrophy.

Source link: https://doi.org/10.1186/s13578-021-00668-4


MicroRNA-30b-5p is Involved in the Regulation of Cardiac Hypertrophy by Targeting CaMKIIδ

Ca 2+/calmodulin-dependent protein kinase II is a hypertrophic signaling component. Purpose: In this research, we found which miRNAs could influence CaMKIIII, including how to monitor CaMKIII. . u03b4 and how to control CaMKIIIu03b4. MiR-30b-5p, according to a Luciferase reporter assay, could significantly reduce the expression of CaMKIII. u03b4 in CaMKIII. u03b4. In addition, we found miR-30b-5p could negatively regulate the expression of CaMKIIII, u03b4 and miR-30b-5p in cardiac hypertrophy by gain-of-function and loss-of-function techniques. MiR-30b-5p is down-regulated in cardiac hypertrophy, and restoration of its function delays the expression of CaMKIII u03b4, meaning that miR-30b-5p may be a hypertrophic suppressor.

Source link: https://doi.org/10.2310/jim.0b013e3182819ac6


Guanosine Triphosphatase Activation Occurs Downstream of Calcineurin in Cardiac Hypertrophy

In the hopes of providing clinical assistance, there is a great deal of interest in deciphering the mechanisms of maladaptive hypertrophy in cardiac hypertrophy. However, little is known about the interactions u2014if anyu2014between these common signaling molecules in hypertrophic heart disease. We looked at the molecular interactions of these molecules, finding that Rho family triphosphatase signaling occurs either downstream of calcineurin or as a preferred, parallel route. In vitro and in vivo, it has been reported that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition blocks hypertrophy, and we note here that u201cstatin-u201d therapy effectively blocks small G protein mobilization and blunts hypertrophic growth.

Source link: https://doi.org/10.2310/6650.2005.53805


QiShenYiQi Pills, a compound in Chinese medicine, protects against pressure overload-induced cardiac hypertrophy through a multi-component and multi-target mode

Abstract: The present research was designed to investigate the cardiovascular response of a Chinese medicine drug, QiShenYi Pills, and the contributions of its constituents to cardiac hypertrophy in rats. The majority of differentially expressed proteins in the heart of QSYQ-treated rats's rats' metabolism were found to be either metabolic or oxidative stress, according to both experimental and western blot results.

Source link: https://doi.org/10.1038/srep11802


Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling

Accumulating evidence reveals that inflammatory cell activation and release of inflammatory mediators are of utmost importance in these cardiac diseases' pathogenesis. Nevertheless, the roles of innate immune cells and subsequent inflammatory reactions in these processes are poorly understood. In these pathologic processes, we discuss here some of the potential underlying mechanisms of innate immune cell function, including mast cells, macrophages, neutrophils, dendritic cells, eosinophils, dendritic cells, eosinophils, dendritic cells, eosinophils, dendritic cells, eosinophils In experimental models, mast cells, neutrophils, and dendritic cells all have detrimental function, but eosinophils and natural killer T cells exhibit cardioprotective activity, among them. Pressure overload increases the persistence of cytokines, chemokines, and growth factors from innate immune cells and even resident cardiomyocytes, which all aid in injury cell infiltration into the injured heart. Immune stimulation of cardiac innate immune cells is a promising therapeutic intervention in experimental cardiac disease therapy, emphasizing the importance of their clinical testing in humans.

Source link: https://doi.org/10.3389/fcell.2021.659666


Lineage-specific regulatory changes in the pathological cardiac remodeling of hypertrophy cardiomyopathy unraveled by single-nucleus RNA-seq and spatial transcriptomics

ABSTRACT BACKGROUND Hypertrophy cardiomyopathy is the most common cardiac genetic disorder with the histopathologic signs of cardiomyocyte hypertrophy and cardiac fibrosis. The myocardium of HCM patients' patients may lead to heart failure and death. A thorough knowledge of the cell type-specific shifts in HCM's pathological cardiac remodeling is vital in designing effective medical drugs to prevent or mitigate the disease's progression. METHODS We performed single-nucleus RNA-seq of the cardiac tissues from ten HCM patients and two healthy donors, as well as spatial transcriptomic assays of 4 cardiac tissue sections from 3 HCM patients. A systematic review was carried out to investigate the lineage-specific shifts in expression profile, subpopulation composition, and intercellular communication in HCM patients' cardiac tissues. We prioritized candidate therapeutic targets for combating the progression to heart failure or attenuating the cardiac fibrosis in HCM based on the findings of independent studies, including pseudotime ordering, differential expression analysis, and differential regulatory network analysis. We investigated the spatial distributions of the key candidate genes, pathways, and subpopulations using the spatial transcriptomic results. Many FGF12, IL31RA, BDNF, S100A1, CRYAB, and PROS1 were among the candidate target genes for mitigating the progression to heart failure in HCM. RUNX1, MEOX1, AEBP1, LEF1, and NRXN3 were among the fibroblast activation targets that were also discovered, and candidate targets for attenuating the cardiac fibrosis in HCM were also identified, as well as RUNX1, MEOX1, AEBP1, LEF1, and NRXN3.

Source link: https://doi.org/10.1101/2021.07.21.453191


Aberrant Splicing Promotes Proteasomal Degradation of L-type CaV1.2 Calcium Channels by Competitive Binding for CaVβ Subunits in Cardiac Hypertrophy

A splice version of Ca V 1. 2 channel with a mutually exclusive exons 21 and 22 was discovered in rodents, Ca V 1. 2 e21+22. Although this version did not feature Ca 2+ ions, it reduced the cell-surface expression of wild-type Ca V 1. 2 channels and subsequently reduced the whole-cell Ca 2+ influx via the Ca V 1. 2 channels, although this version did not have Ca 2+ ions. The Ca V 1. 2 e21+22 variant in addition enhanced ubiquitination and subsequent proteasomal degradation of the wild-type Ca V 1. 2 channels, as well as wild-type Ca V 1. 2 channels. The revival of a specific neonatal splice version of Ca V 1. 2 channels in adult heart under strain could contribute to heart failure, according to our results.

Source link: https://doi.org/10.1038/srep35247

* 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