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Cardiac Hypertrophy - DOAJ

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Last Updated: 10 January 2023

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

Background Cardiomegaly induced by left ventricular hypertrophy is a risk factor for congestive heart disease, which is traditionally associated with reduced systolic and/or diastolic ventricular function. The phenotype of left ventricular hypertrophy with improved ventricular function and increased cardiac output, which could be potentially related to higher-output heart failure, according to a high u2010 output heart failure. We investigated the cardiovascular phenotype longitudinally in 31 individuals with confirmed ABCC9 variants in 31 subjects with confirmed ABCC9 variants. With normal left ventricular wall thickness, most CS patients with eccentric hypertrophy developed eccentric hypertrophy. In 4 of the 5 patients with CS aged > 40 years on long-term follow-up, heart failure symptoms were present. Conclusions: The data reveal the natural history of high-output heart hypertrophy in subjects with CS, a defining population for long-u2013 cardiovascular failure owing to low systemic vascular resistance, and the possibility of progression to high-output heart failure due to poor systemic vascular resistance.

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


Rg3 regulates myocardial pyruvate metabolism via P300-mediated dihydrolipoamide dehydrogenase 2-hydroxyisobutyrylation in TAC-induced cardiac hypertrophy

Abstract The declining heart is characterized by an rise in glucose uptake and glycolytic rates that is not followed by a concomitant rise in glucose oxidation. Lower coupling of glucose oxidation to glycolysis may be due to unchanged or reduced pyruvate oxidation in mitochondria. Hence, increasing pyruvate oxidation may lead to new heart disease treatments. However, no studies have investigated the effects of DLD mutants or acylation status on PDH production and pyruvate metabolism. The 2-hydroxyisobutylation of DLD in a mouse model of transverse aortic constriction-induced cardiac hypertrophy was significant, owing to a decrease in PDH levels. As one of the key active ingredients of ginseng, ginsenoside Rg3 can reduce DLD's 2-hydroxyisobutylation levels and PDH regrowth by reducing PDH production when the heart is injured, thus providing therapeutic benefits whenever the heart is injured.

Source link: https://doi.org/10.1038/s41419-022-05516-y


Prostaglandin E2 induced cardiac hypertrophy through EP2 receptor‐dependent activation of β‐catenin in 5/6 nephrectomy rats

Methods and findings We investigated the effect of PGE2 receptor inhibitors on cardiac hypertrophy in vitro and in a 5/6 nephrectomy rat model using quantitative reverse transcription polymerase chain reaction, western blotting, enzyme-u2010linked immunosorbent assay, immunohistochemical staining, and immunofluorescence staining assays. PGE2 in the 5/6NT rat model was found for 2 weeks, prompting the discovery of the PGE2 in the 5/6NT rat model. In 5/6NT rats, EP2 receptor inhibitor therapy significantly improved the cardiac function and fibrosis. 5/6NT rats' heart hypertrophy could be improved by inhibition of EP2 receptor, according to the study.

Source link: https://doi.org/10.1002/ehf2.13269


FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy

Abstract Background: Abstract Background Sustained cardiac hypertrophy often leads to dysfunctional myocardial remodeling, which then progresses to heart failure and sudden death. Therefore, maladaptive hypertrophy is considered a significant therapeutic target for several heart diseases. Mitophagy, a crucial component of mitochondria quality control and cellular homeostasis, has been implicated in various cardiac diseases including myocardial infarction, diabetic cardiomyopathy, cardiac hypertrophy, and heart failure. However, what role mitophagy plays in heart disease remains an enigma. PARKIN is a member of the E3 ubiquitin protein ligase and mediates mitophagy cascades in the United States. It is also unknown if PARKIN is involved in the oversight of cardiac hypertrophy. PARKIN-inhibited cardiomyocyte hypertrophy was reduced in Enforced Ang II-induced cardiomyocyte hypertrophy. Compared to wide-type mice with Ang II-induced cardiac hypertrophy, Parkin transgenic mice treated to Ang II stimulation showed reduced cardiac hypertrophy and improved cardiac function. By attacking Parkin, FOXO3a promoted mitophagy and reduced cardiac hypertrophy.

Source link: https://doi.org/10.1186/s13578-022-00935-y


The protective effect of Apelin-13 against cardiac hypertrophy through activating the PI3K-AKT-mTOR signaling pathway

The control group, the PE group, the PE+Apelin group, the PE+Rapa company, and the PE+Apelin+Rapa group were divided into five groups separately: the H9C2 and Si-APJ cells were divided into five groups: the PE group, the PE group, the PE+Apelin group, and the PE+Apelin+Rapa group were divided into five groups: the control group, the PE group, the PE+Apelin group, MYH7 was significantly higher in the PE group in comparison to the PE+Apelin group in H9C2 cells, indicating that the expression of the PI3K/AKT/mTOR pathway proteins and MYH7 was significantly higher in the PE group relative to the PE+Apelin group. The expression of MYH7 protein in the PE group was elevated in H9C2 cells in comparison to the control group. MYH7 expression in the PE group, in Si-APJ H9C2 cells, compared to the control group, was nonetheless high. Conclusion: Apelin-13 reduces PE-induced cardiac hypertrophy in the PE+Apelin, PE+Rapa, and PE+Apelin+Rapa groups by activating the PI3K/mTOR signaling pathway in the same cell line, while the PE+Apelin-13 group does not have a statistically significant difference in MYH7 expression between the PE+Apelin, PE+Rapa, and PE+Apelin+Rapa groups, compared to the PE-MTOR signaling the mTOR trophy in cerebral hypertrophy in the PE+Apelin trophy in the trophy in the PE+Rapa a mTOR signaling the mTOR signaling pathway, Apelin-MTOR signaling pathway mTOR signaling pathway, according to the PE+Apelin-B/MTOR signaling pathway in the PE+Amelin versus the PE+Rapa, Apelin-Amelin-Apelin-MTOR gene expression in the PE+At.

Source link: https://doi.org/10.22038/ijbms.2022.65160.14356


Andrographolide contributes to the attenuation of cardiac hypertrophy by suppressing endoplasmic reticulum stress

Objective: This paper investigates Andr's results and underlying mechanism of cardiac hypertrophy in mice, including a sham group, transverse aortic constriction model group, TAC + Andr 100 mg/kg group, and TAC + Andr 200 mg/kg group. Andr groups in Andr were given intragastric administration of Andr for the 14 days in a row. Andr attenuated cardiomyocyte hypertrophy and decreased the protein expression of GRP78, GRP94, p-PERK, and CHOP in Ang-III-induced H9c2 cells, which was reversed after endoplasmic reticulum stress agonist Tunicamycin treatment. Physiological regulator Andr was found to be an anti-hypertrophic regulator, with an agonist of cardiac hypertrophy and decreased cardiac hypertrophy and reduced cardiac trophy and Toxitrophy and reduced cardiac hypertrophy and reduced the expression of THI, THIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII.

Source link: https://doi.org/10.1080/13880209.2022.2157021


Cardiac Hypertrophy and Related Dysfunctions in Cushing Syndrome Patients—Literature Review

Because of the availability of appropriate surgical and pharmacological drugs, the survival rate of adrenal Cushing syndrome patients has greatly increased. However, the increased likelihood of a heart attack triggered by a cardiovascular disease remains a significant risk factor for the survival of affected patients. Hypercortisolemia has been shown to cause cardiomyocyte hypertrophy in experimental studies, as well as the possibility of cross talk among several hypertrophic signals related to cardiomyocytes and tissue-specific control of 11–u03b2-hydroxysteroid dehydrogenase type 1 and tissue-dependent regulation of 11–u03b2-hydroxysteroid dehydrogenase type 1.

Source link: https://doi.org/10.3390/jcm11237035


Aging Increases Susceptibility to Develop Cardiac Hypertrophy following High Sugar Consumption

Heart disease risk factors are aging and poor diet, according to the authors, but the effects of high-sucrose consumption in the elderly heart is understudied. In 24-month-old male CB6F1 mice, we investigated whether HS diet would promote muscle deficion. Mice on the HS diet had significant cardiac hypertrophy by week 1 in comparison to age-matched chow-fed controls. We then investigated whether HS diet could exacerbate cardiac disease in old mice, and if the mitochondrial-targeted drug, elamipretide, could avoid the diet-induced side effects. Old mice had age-related cardiac hypertrophy that worsened after one week on HS and was prevented by ELAM therapy, as shown by the previous study, while the HS diet had no effect on hypertrophy in the young mice. Our results reveal that the aged heart is vulnerable to a HS diet, which can be prevented by systemic targeting of mitochondria with ELAM.

Source link: https://doi.org/10.3390/nu14214645


Administration of USP7 inhibitor P22077 inhibited cardiac hypertrophy and remodeling in Ang II-induced hypertensive mice

Hypertension is one of the most common causes of pathological cardiac hypertrophy and a significant risk of cardiovascular disease and mortality worldwide. Our results showed that USP7 expression was up during Ang II-induced cardiac hypertrophy and remodeling in mice and humans with heart failure, while its inhibitor p22077 reduced cardiac hypertrophy and inflammation, cardiac fibrosis, inflammation, and oxidase stress, which were normalized here. These results, taken together, indicate that USP7 may be a new therapeutic target for hypertrophic remodeling and HF.

Source link: https://doi.org/10.3389/fphar.2022.1021361


Multiple short‐chain dehydrogenases/reductases are regulated in pathological cardiac hypertrophy

Cardiac hypertrophy is a vital and reliable predictor of morbidity and mortality. All but Hsd11b1 were downregulated in CH models, according to nine SDR genes tested. We found that the phenylephrine treatment in neonatal rat cardiomyocytes mostly matched the observations obtained in CH animal models. Retinoic acid, on the other hand, stimulated the expression of major SDR genes studied's genes, indicating that their expression may be related to cardiomyocyte differentiation. In conclusion, we found a line of genes that were altered in animal models of CH, mostly in males. This may be due to the initiation of the fetal gene expression program in pathological CH conditions, in which these highly expressed genes are downregulated in the adult heart.

Source link: https://doi.org/10.1002/2211-5463.12506

* 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