β-Adrenoceptor activation affects galectin-3 as a biomarker and therapeutic target in heart disease.

摘要: Myocardial fibrosis is a key histopathological component that drives the progression of heart disease leading to failure and constitutes therapeutic target. Recent preclinical clinical studies have implicated galectin-3 (Gal-3) as pro-fibrotic molecule biomarker fibrosis. However, our knowledge poor on mechanism(s) determine blood level or regulate cardiac expression Gal-3. demonstrated enhanced β-adrenoceptor activity determinant both circulating concentration Pharmacological transgenic activation β-adrenoceptors leads increased levels Gal-3 up-regulated expression, effect can be reversed with use antagonists. Conversely, gene deletion confers protection against isoprenaline-induced cardiotoxicity fibrogenesis. At transcription level, stimulation activates mammalian sterile-20-like kinase 1, pivotal Hippo signalling pathway, which associated up-regulation. suggested role for β-adrenoceptor-Hippo pathway in regulation thereby contributing onset disease. This implies potential suppression expression. In this review, we discuss effects causative mediator setting point out gaps. LINKED ARTICLES: article part themed section Adrenoceptors-New Roles Old Players. To view other articles visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.14/issuetoc.