As heart failure (HF) is a growing public health problem worldwide, rapid therapeutic development is required to improve HF management. Decreased myocardial contractility in HF is associated with the persistent sympathetic activation of β1/β2-adrenoceptors (β1/β2-ARs). Although it is initially activated to compensate for a decline in myocardial contractility, it plays a pivotal role in organ damage and functional deterioration over time, resulting in the desensitization of receptors involved. The third β-AR subtype, β3-AR, is resistant to desensitization, and as a result, the expression of this subtype is enhanced in human failing myocardium. In addition, this upregulation and the stimulation of this subtype have been demonstrated to mediate cardioprotective effects such as antihypertrophic, antioxidant and antifibrotic effects via various signaling pathways in different cell types. However, the role of this attractive therapeutic intervention in heart diseases must be clarified through clinical trials.
Keywords: Heart failure; Nitric oxide; β(3)-AR.
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