Key result
Chronic catecholamine stimulation of beta-adrenoceptors mediates adverse myocardial remodeling and heart failure through various signaling pathways.
A full understanding of beta-AR-mediated cardiac remodeling mechanisms could indicate novel therapeutic targets for heart failure.
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Supports beta-blocker use in HF; leaves open pathway-specific targets for novel therapies.
Beta-adrenoceptors (ARs), members of the G protein-coupled receptor (GPCR) superfamily, play a key role in the rapid regulation of myocardial function. Meanwhile, chronic catecholamine stimulation of adrenoceptors has been proved to be involved in the adverse myocardial remodeling, including cardiac hypertrophy, fibrosis, and apoptosis, which finally develop into heart failure. In the clinical situation, sympathetic hyperactivity is a key factor in the development of heart failure, and beta-blockers greatly improve the outcome of the disease. However, heart failure is still one of the leading causes of death. Therefore, a full understanding of the mechanism of beta-AR-mediated cardiac remodeling could indicate more targets for treating heart failure. This review summarizes a number of important signaling pathways involved in the process of cardiac pathological remodeling under chronic adrenergic stimulation.
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Yongnan Fu (2011) conducted a review in Heart failure and cardiac pathological remodeling. Chronic adrenergic stimulation was evaluated. Chronic catecholamine stimulation of beta-adrenoceptors mediates adverse myocardial remodeling and heart failure through various signaling pathways.
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