Heart failure (HF) is characterized by notable alterations in β-adrenergic receptor (β-AR) signaling. It is well known that a prolonged overstimulation of β-ARs, a member of the G-protein-coupled receptor (GPCR) family, alters receptor density and function, contributing to cardiac dysfunction and the development and progression of HF. Moreover, recently, many studies have highlighted the role of β-ARs in the regulation of mitochondrial fission/fusion. A dysfunctional mitochondrial fission/fusion balance is a characteristic hallmark of a failing heart. However, a mechanistic link between β-ARs and mitochondrial dynamics is lacking. Furthermore, growing evidence links β-AR activity to changing mitochondrial size, distribution, and functional integrity. Yet these findings remain scattered across diverse studies with differing perspectives. This review demonstrates a clear mechanistic view of β-ARs regulation of mitochondrial fission/fusion in a failing heart.
Panchbhai et al. (2026) studied this question.