Activation of β2 adrenergic receptor signaling modulates inflammation: a target limiting the progression of kidney diseases

Beta 2 adrenergic receptor (beta(2)-AR)-agonists, widely used as bronchodilators, have demonstrated wide-spectrum anti-inflammatory properties in both immune and non-immune cells in various tissues. Their anti-inflammatory properties are mediated primarily, but not exclusively, via activation of the canonical beta(2)-AR signaling pathway (beta(2)-AR/cAMP/PKA). As non-canonical beta(2)-AR signaling also occurs, several inconsistent findings on the anti-inflammatory effect of beta(2)-agonists are notably present. Increasing amounts of evidence have unveiled the alternative mechanisms of the beta(2)-AR agonists in protecting the tissues against injuries, i.e., by augmenting mitochondria biogenesis and SIRT1 activity, and by attenuating fibrotic signaling. This review mainly covers the basic mechanisms of the anti-inflammatory effects of beta(2)-AR activation along with its limitations. Specifically, we summarized the role of beta(2)-AR signaling in regulating kidney function and in mediating the progression of acute and chronic kidney diseases. Given their versatile protective effects, beta(2)-agonists can be a promising avenue in the treatment of kidney diseases.

Automated summary

Beta 2 adrenergic receptor (β(2)-AR) agonists, commonly used as bronchodilators, have broad-spectrum anti-inflammatory properties by activating the canonical β(2)-AR signaling pathway. Inconsistent findings on their anti-inflammatory effects are attributed to non-canonical β(2)-AR signaling. These agonists also protect tissues from injury by mechanisms such as increasing mitochondria biogenesis and SIRT1 activity, and attenuating fibrotic signaling. Beta(2)-agonists show promise in treating kidney diseases due to their versatile protective effects.