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Activation of beta(2) adrenergic receptor signaling modulates inflammation: a target limiting the progression of kidney diseases
- Title
- Activation of beta(2) adrenergic receptor signaling modulates inflammation: a target limiting the progression of kidney diseases
- Authors
- Dorotea, Debra; Ha, Hunjoo
- Ewha Authors
- 하헌주
- SCOPUS Author ID
- 하헌주
- Issue Date
- 2021
- Journal Title
- ARCHIVES OF PHARMACAL RESEARCH
- ISSN
- 0253-6269
1976-3786
- Citation
- ARCHIVES OF PHARMACAL RESEARCH vol. 44, no. 1, pp. 49 - 62
- Keywords
- β (2)-Adrenergic receptors; (2)-Agonist; Cyclic AMP; GPCR; Inflammation; Kidney diseases
- Publisher
- PHARMACEUTICAL SOC KOREA
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Review
- Abstract
- 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.
- DOI
- 10.1007/s12272-020-01280-9
- Appears in Collections:
- 약학대학 > 약학과 > Journal papers
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