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β肾上腺素能受体信号的激活调节炎症:限制肾脏疾病进展的靶点。

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

机构信息

Graduate School of Pharmaceutical Sciences, College of Pharmacy, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul, 03760, Republic of Korea.

出版信息

Arch Pharm Res. 2021 Jan;44(1):49-62. doi: 10.1007/s12272-020-01280-9. Epub 2020 Nov 5.

DOI:10.1007/s12272-020-01280-9
PMID:33155167
Abstract

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

摘要

β2 肾上腺素能受体(β-AR)激动剂被广泛用作支气管扩张剂,已在各种组织的免疫和非免疫细胞中显示出广谱的抗炎特性。它们的抗炎特性主要但并非完全通过激活经典的β-AR 信号通路(β-AR/cAMP/PKA)来介导。由于也存在非经典的β-AR 信号,β-激动剂的抗炎作用存在一些不一致的发现。越来越多的证据揭示了β-AR 激动剂在保护组织免受损伤方面的替代机制,即通过增加线粒体生物发生和 SIRT1 活性,并减弱纤维化信号。本综述主要涵盖了β-AR 激活的抗炎作用的基本机制及其局限性。具体而言,我们总结了β-AR 信号在调节肾脏功能和介导急性和慢性肾脏疾病进展中的作用。鉴于其多功能的保护作用,β-激动剂可能是治疗肾脏疾病的一个有前途的途径。

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