8/26/2023 0 Comments Pathological hypertrophy heart![]() C/EBPβ controls exercise-induced cardiac growth and protects against pathological cardiac remodeling. The FOXO3a transcription factor regulates cardiac myocyte size downstream of AKT signaling. Phosphoinositide 3-kinase(p110α) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy. The insulin-like growth factor 1 receptor induces physiological heart growth via the phosphoinositide 3-kinase(p110α) pathway. Insulin receptor substrates are essential for the bioenergetic and hypertrophic response of the heart to exercise training. Distinct signaling by insulin and IGF-1 receptors and their extra- and intracellular domains. New insights into IGF-1 signaling in the heart. the failing heart: Can signaling explain the two distinct outcomes? Physiology 26, 97–105 (2011). Mechanisms of physiological and pathological cardiac hypertrophy. Dynamics of cell generation and turnover in the human heart. Cardiac hypertrophy: molecular and cellular events. eccentric remodelling in heart failure with reduced ejection fraction: clinical characteristics, pathophysiology and response to treatment. Regression of left ventricular mass in athletes undergoing complete detraining is mediated by decrease in intracellular but not extracellular compartments. Left ventricular hypertrophy in athletes. Reverse remodelling and myocardial recovery in heart failure. NT-proBNP goal achievement is associated with significant reverse remodeling and improved clinical outcomes in HFrEF. Effect of left ventricular reverse remodeling on long-term outcomes after aortic valve replacement. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. The MESA (Multi-Ethnic Study of Atherosclerosis) study. ![]() The relationship of left ventricular mass and geometry to incident cardiovascular events. The leading causes of death in the US for 2020. The potential for reverse remodelling in heart disease is influenced by many factors, including biological sex, genetics, duration of hypertension, BMI, age and disease aetiology.Įxercise-induced and pregnancy-induced physiological cardiac hypertrophy is driven by cellular mechanisms distinct from those in pathological hypertrophy, and is completely reversible, whereas moderate exercise in heart failure antagonizes pathological cellular pathways and promotes hypertrophy regression.Īt the molecular level, hypertrophy regression is associated with metabolic shifts, reduced protein synthesis, extracellular matrix remodelling and altered activity of proteolytic pathways.Īhmad, F. Partial reversal of cardiac hypertrophy occurs with many existing heart failure therapies, including renin–angiotensin–aldosterone system, β-adrenergic receptor, calcium-channel and SGLT2 antagonists, but is achieved in only a subset of patients. Pathological cardiac hypertrophy is a leading risk factor for cardiovascular morbidity and mortality and is associated with increased fibrosis and apoptosis that lead to ventricular stiffness, risk of arrhythmia and impaired cardiac function. We further discuss the molecular features of reverse remodelling identified in cell and animal models, highlighting remaining knowledge gaps and the essential questions for future investigation towards the goal of designing specific therapies to promote regression of pathological hypertrophy. In this Review, we summarize the evidence for hypertrophy regression in patients with current first-line pharmacological and surgical interventions. Studies over the past decade have identified the molecular features of hypertrophy regression in health and disease settings, which include modulation of protein synthesis, microRNAs, metabolism and protein degradation pathways. Cardiac hypertrophy also occurs in physiological settings, including pregnancy and exercise, although in these cases, hypertrophy is associated with normal or improved ventricular function and is completely reversible postpartum or with cessation of training. However, less than 50% of patients respond favourably to most therapies, and the reversibility of remodelling is influenced by many factors, including age, sex, BMI and disease aetiology. The regression of pathological hypertrophy is associated with improved cardiac function, quality of life and long-term health outcomes. Although reverse ventricular remodelling was long thought to be irreversible, evidence from the past three decades indicates that this process is possible with many existing heart disease therapies. Left ventricular hypertrophy is a leading risk factor for cardiovascular morbidity and mortality.
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