纤维化
下调和上调
受体
体内
脂联素
癌症研究
信号转导
医学
脂联素受体1
药理学
内科学
生物
细胞生物学
基因
生物技术
胰岛素抵抗
胰岛素
生物化学
作者
Lingman Ma,Xuanyi Li,Zhaoshi Bai,Xinhao Lin,Kejiang Lin
标识
DOI:10.1080/14728222.2019.1559823
摘要
Introduction: Fibrotic disorders are a leading cause of morbidity and mortality; hence effective treatments are still vigorously sought. AdipoRs (AdipoR1 and Adipo2) are responsible for the antifibrotic effects of adiponectin (APN). APN exerts antifibrotic effects by binding to its receptors. APN concentration and AdipoR expression are closely associated with fibrotic disorders. Decreased AdipoR expression may reduce APN-AdipoR signaling, while the upregulation of AdipoR expression may restore the anti-fibrotic effects of APN. Loss of APN signaling exacerbates fibrosis in vivo and in vitro. Areas covered: We assess the relationship between APN and fibrotic disorders, the structure of receptors for APN and the pathways accounting for APN or its analogs blocking fibrotic disorders. This article also discusses designed APN products and their therapeutic prospects for fibrotic disorders. Expert opinion: AdipoRs have a critical role in blocking fibrosis. The development of small-molecule agonists toward this target represents a valid drug development pathway.
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