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Cardiac Hypertrophy - Europe PMC

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Last Updated: 10 January 2023

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

Objectives This paper explores Andr's effectiveness and underlying mechanism of cardiac hypertrophy in mice. Materials and methods Male C57 mice were divided into four groups as a sham group, transverse aortic constriction model group, TAC + Andr 100 mg/kg group, and TAC + Andr 200 mg/kg group. Andr groups were administered intragastric administration of Andr for the first day in 14 days. For 48 h induction, An in vitro hypertrophy model was developed by adding 1 bcM of Ang II to H9c2 cells. Andr's TAC mice had improved echocardiographic indices [reduced LVESD and LVEDD, raised EF and FS], reduced BNP and Ang II levels, attenuates cardiac fibrosis, and reduced cardiac cell apoptosis, and reduced cardiac cell apoptosis.

Source link: https://europepmc.org/article/MED/36548192


Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.

Left ventricular hypertrophy is a common risk factor for cardiovascular morbidity and mortality. Although reverse ventricular remodelling was long thought to be irreversible, recent heart disease research shows that this process is also possible with several existing heart disease treatments. Pathological hypertrophy's reversal is correlated with improved cardiac function, quality of life, and long-term health effects. Cardiac hypertrophy also occurs in physiological conditions, such as pregnancy and exercise, although in those situations, hypertrophy is restricted to improved ventricular function and is unquestionably reversible postpartum or training interruptions. The molecular characteristics of hypertrophy reduction in health and disease settings, which include alterations in protein synthesis, microRNA, metabolism, and protein degradation pathways, have been determined by researchers over the past decade. In this Review, we summarize the findings for hypertrophy recovery in patients with current first-line pharmacologic and surgical interventions.

Source link: https://europepmc.org/article/MED/36596855


Calanus oil attenuates isoproterenol-induced cardiac hypertrophy by regulating myocardial remodeling and oxidative stress.

Calanus oil, which is an oil extracted from the marine crustacean Calanus finmarchicus, is one of the finest sources of omega-3 and poly-unsaturated fatty acids. Although calanus oil has been shown to have potent anti-hypertensive, anti-inflammatory, anti-fibrotic, and anti-obesity properties in various cardiovascular disorders, few details about its effects on pathological cardiac hypertrophy have been published. The present study was done to determine the calanus oil's therapeutic effect on cardiac hypertrophy. Cardiac hypertrophy was induced by subcutaneous injections of isoproterenol for 14 days in a row. The Calanus oil was used orally for four weeks. Calanus oil also reduced the relative heart weight, dramatically reduced the elevated cardiac enzymes and the lipid peroxidation marker, boosted the myocardial antioxidant status, enhanced the myocardial antioxidant status, and prevented interstitial collagen deposition by reducing interstitial collagen deposition. This anti-hypertrophic effect of calanus oil is due to the restriction of myocardial remodeling and oxidative stress.

Source link: https://europepmc.org/article/MED/36588172


Does Vitamin D Provide Added Benefit to Antihypertensive Therapy in Reducing Left Ventricular Hypertrophy Determined by Cardiac Magnetic Resonance?

Background Left ventricular hypertrophy and vitamin D deficiency have been attributed to hypertension and cardiovascular disease, particularly in African Americans. After 1 year in vitamin D deficient AA patients with uncontrolled HTN and LVH, we decided that adding vitamin D to antihypertensive therapy would result in more LV mass index decline. The vitamin D and placebo groups had no statistical differences in LVMI or systolic BP reductions, respectively, at 1 year. Vitamin D levels in the vitamin D group increased sharply in comparison to placebo. Conclusions: We did not find a correlation between vitamin D supplementation and variable LVMI or reduction in systolic BP in this high-risk cohort of AAs.

Source link: https://europepmc.org/article/MED/36008108


Effect of inflammation on cytochrome P450-mediated arachidonic acid metabolism and the consequences on cardiac hypertrophy.

The enlargement of cardiac myocytes in response to stress is often preceded by heart failure by cardiac hypertrophy, which is the enlargement of cardiac myocytes in response to stress. We're trying to highlight the effect of inflammation on CYP-derived AA metabolites and CH in this study. Inflammation has been shown to regulate the expression of various CYP u03c9-hydroxylases and CYP epoxygenases as well as their respective metabolites in the heart. This research examined the inflammatory modulation of cardiac CYPs and their metabolites in the context of CH and the use of anti-inflammatory agents in CH and HF's therapy.

Source link: https://europepmc.org/article/MED/36573379


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

An rise in glucose uptake and glycolytic rates that is not followed by a concomitant rise in glucose oxidation is characteristic of the failing heart. Lower coupling of glucose oxidation to glycolysis may be due to unchanged or reduced pyruvate oxidation in mitochondria. Therefore, increasing pyruvate oxidation could lead to new heart disease treatments. Dihydrolipoamide dehydrogenase, which is a component of the pyruvate dehydrogenase complex, is a component. However, few studies have investigated the effects of DLD mutants or acylation status on PDH production and pyruvate metabolism. However, there are no published studies on the effect of 2-hydroxyisobutyrylation on heart failure's energy metabolism, and it deserves more in-depth research. ginsenoside Rg3 can reduce the 2-hydroxyisobutylation levels of DLD and restore PDH activity by reducing the acyltransferase enzyme activity of P300, resulting in beneficial effects wherever the heart is injured.

Source link: https://europepmc.org/article/MED/36572672


Palmitic acid methyl ester induces cardiac hypertrophy through activating the GPR receptor-mediated changes of intracellular calcium concentrations and mitochondrial functions.

However, PAME's effects on cardiomyocytes are still unclear. This research was designed to see if PAME could alter the intracellular Ca 2+ balance, causing cardiomyocyte hypertrophy. For 1-4 days, Neonatal rat cardiomyocytes were treated with various PAME concentrations for Neonatal rat cardiomyocytes. Cell death was measured by flow cytometry analysis after PAME therapy for four days, mitochondrial Ca 2+, an indicator of mitochondrial permeability transition pore state, and cell death. Using quantitative real time-polymerase chain reaction, Western Blot analysis, and immunofluorescence analysis, cardiomyocyte hypertrophy was investigated by investigating the cardiac hypertrophy biomarker and cell area. PAME concentration- and time-dependently increased cytosolic and mitochondria Ca 2+ by the mitochondrial calcium uniporter, according to our findings. In conclusion, PAME impaired mitochondrial function, which in turn resulted in cardiomyocyte hypertrophy, which in turn resulted in cardiomyocyte hypertrophy by raising the mitochondrial Ca 2+ levels mediated by activating the GPR40 signaling pathway.

Source link: https://europepmc.org/article/MED/36538623


FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy.

Consequently, maladaptive hypertrophy has been identified as a key therapeutic target for several heart diseases. Mitophagy, a vital component of mitochondria quality control and cellular homeostasis, has been implicated in numerous 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 mitochondrial cascades. It is now unknown if PARKIN is involved in cardiac hypertrophy regulation. PARKIN's controlled expression of Enforced Ang II-induced cardiomyocyte hypertrophy was blocked by Enforced cell proliferation. Compared to wide-type mice with Ang II-induced cardiac hypertrophy, Parkin transgenic mice treated to Ang II treatment demonstrated decreased cardiac hypertrophy and improved cardiac function. PARKIN promoted mitophagy, resulting in the anti-hypertrophy effect. FOXO3a, a drug that aims Parkin, promoted mitophagy and slowed cardiac hypertrophy. Modulation of their blood sugar levels can be a new way to prevent cardiac hypertrophy and heart failure.

Source link: https://europepmc.org/article/MED/36539848


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

Background Cardiomegaly caused by left ventricular hypertrophy is a risk factor for congestive heart failure, which is generally associated with reduced systolic and/or diastolic ventricular function. Left ventricular hypertrophy with enhanced ventricular function and elevated cardiac output, which may be due to heart failure and high output heart failure, has dragged Less' attention. We investigated the cardiovascular phenotype longitudinally in 31 patients with confirmed ABCC9 variants in 31 patients with confirmed ABCC9 variants. Normal left ventricular wall thickness was observed in the majority of subjects with CS eccentric hypertrophy. In 4 of the 5 patients with CS older than 40 years on long-term follow-up, heart failure symptoms were evident. Conclusions The results reveal the natural history of high-output hypertrophy in people with CS, a defining population for long-term consequences of high-output hypertrophy owing to low systemic vascular resistance, as well as the possibility of progression to high-output heart failure.

Source link: https://europepmc.org/article/MED/36515236

* 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