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KMID : 0043320210440010049
Archives of Pharmacal Research
2021 Volume.44 No. 1 p.49 ~ p.62
Activation of ¥â2 adrenergic receptor signaling modulates inflammation: a target limiting the progression of kidney diseases
Dorotea Debra

Ha Hun-Joo
Abstract
Beta 2 adrenergic receptor (¥â2-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 ¥â2-AR signaling pathway (¥â2-AR/cAMP/PKA). As non-canonical ¥â2-AR signaling also occurs, several inconsistent findings on the anti-inflammatory effect of ¥â2-agonists are notably present. Increasing amounts of evidence have unveiled the alternative mechanisms of the ¥â2-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 ¥â2-AR activation along with its limitations. Specifically, we summarized the role of ¥â2-AR signaling in regulating kidney function and in mediating the progression of acute and chronic kidney diseases. Given their versatile protective effects, ¥â2-agonists can be a promising avenue in the treatment of kidney diseases.
KEYWORD
¥â2-Adrenergic receptors, ¥â2-Agonist, Cyclic AMP, GPCR, Inflammation, Kidney diseases
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