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Cardiac Hypertrophy - Springer Nature

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Last Updated: 10 January 2023

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

Pathological cardiac hypertrophy is the most common risk factor for cardiovascular morbidity and mortality, and it is associated with increased fibrosis and apoptosis, which contribute to ventricular stiffness, risk of arrhythmia, and impaired cardiac function. Partial reversal of cardiac hypertrophy is achieved with many existing heart failure treatments, including the renin-u2013angiotensin, u03b2-adrenergic receptor, calcium-channel, and SGLT2 antagonists, but only in a small number of patients. Many variables, including genetics, duration of hypertension, BMI, age, and disease aetiology, can influence heart disease reversibility reverse remodelling. Exercise-induced and pregnancy-induced physiological hypertrophy is triggered by genes specific to pathological hypertrophy and is reversible, while moderate exercise in heart failure antagonizes pathological cellular pathways and promotes hypertrophy regression. Left ventricular hypertrophy is a common risk factor for cardiovascular morbidity and mortality. Although reverse ventricular remodelling was long thought to be irreversible, studies from the last three decades show that this process is achievable with several common heart disease therapies. Cardiac hypertrophy also occurs in physiological conditions, such as pregnancy and exercise, but in those situations, hypertrophy is mainly reversible postpartum or training abandonment. In this Review, the authors summarize the evidence for physiological and pathological hypertrophy regression from clinical and basic science research, discussing drugs and mechanisms involved in cardiac hypertrophy regression, stressing knowledge gaps and needing innovative therapies to promote pathological hypertrophy recovery.

Source link: https://doi.org/10.1038/s41569-022-00806-6


Quercetin: A Promising Flavonoid for the Therapy of Cardiac Hypertrophy and Heart Failure Mediated by the Renin Angiotensin System

Maintaining cardiovascular homeostasis is a key component of the Renin angiotensin II regime and regulating angiotensin II levels in the body and maintaining cardiovascular homeostasis. Cardiac hypertrophy (CD) and other causes cause heart disease, Heart failure is common. One of the main risk factors that causes pathological changes in the coronary blood vessels, often resulting in heart attack and stroke is a high blood pressure that leads to cardiovascular disease. Heart failure, heart disease, and heart failure were all demonstrated by preclinical and limited number of clinical studies. Coronary heart disease, hypertension, myocardial hypertrophy, and heart failure are all reported by quercetin Quercetin's multiple benefits, including ACE inhibition, potent antioxidant and anti-inflammatory activity, and shielding of endothelial function, which collectively prevent coronary heart disease Coronary heart disease Coronary heart disease, hypertension, and heart disease.

Source link: https://doi.org/10.1007/978-3-031-14952-8_23


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 in the failing heart is characterized by an increase 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. Also, increasing pyruvate oxidation may lead to new heart disease treatments. Dihydrolipoamide dehydrogenase is a component of the pyruvate dehydrogenase complex. However, no research has looked at the effects of DLD mutants or acylation status on PDH function and pyruvate metabolism. The 2-hydroxyisobutylation of DLD in a mouse model of transverse aortic constriction-induced cardiac hypertrophy was significant, owing to the decrease in PDH levels. ginsenoside Rg3 can reduce the 2-hydroxyisobutylation levels of DLD and reactivate PDH production by reducing the PDH's activity by blocking P300's acyltransferase production, thereby providing therapeutic effects whenever the heart is injured.

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


FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagy

Sustained cardiac hypertrophy often leads to dysfunctional myocardial remodeling, which leads to heart failure and sudden death. Hence, maladaptive hypertrophy is regarded as a key therapeutic target for several heart diseases. Mitophagy, a key component of mitochondrial quality control and cellular homeostasis, cardiac hypertrophy, and heart failure have been implicated in a variety of cardiac disorders, including myocardial infarction, diabetic cardiomyopathy, cardiac hypertrophy, and heart failure. However, the role that mitochondrial play in heart disease remains an enigma. PARKIN serves as an E3 ubiquitin protein ligase and mediates mitophagy cascades. It is still unclear if PARKIN is involved in cardiac hypertrophy control. Parkin transgenic mice treated to Ang II administration showed attenuated cardiac hypertrophy and improved cardiac function in comparison to wide-type mice with Ang II-induced cardiac hypertrophy. Conclusions The present research reveals a novel cardiac hypertrophy regulating system made up of FOXO3a, PARKIN, and motophagy protocols.

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

* 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