大黄素
成纤维细胞
心脏纤维化
纤维化
转化生长因子
信号转导
细胞生物学
癌症研究
化学
药理学
生物
体外
医学
生物化学
内科学
作者
Wayne Carver,Ethan Fix,Charity Fix,Daping Fan,Mrinmay Chakrabarti,Mohamad Azhar
摘要
Abstract Cardiac fibrosis accompanies a number of pathological conditions and results in altered myocardial structure, biomechanical properties and function. The signaling networks leading to fibrosis are complex, contributing to the general lack of progress in identifying effective therapeutic approaches to prevent or reverse this condition. Several studies have shown protective effects of emodin, a plant‐derived anthraquinone, in animal models of fibrosis. A number of questions remain regarding the mechanisms whereby emodin impacts fibrosis. Transforming growth factor beta 1 (TGF‐β1) is a potent stimulus of fibrosis and fibroblast activation. In the present study, experiments were performed to evaluate the effects of emodin on activation and function of cardiac fibroblasts following treatment with TGF‐β1. We demonstrate that emodin attenuates TGF‐β1‐induced fibroblast activation and collagen accumulation in vitro. Emodin also inhibits activation of several canonical (SMAD2/3) and noncanonical (Erk1/2) TGF‐β signaling pathways, while activating the p38 pathway. These results suggest that emodin may provide an effective therapeutic agent for fibrosis that functions via specific TGF‐β signaling pathways.
科研通智能强力驱动
Strongly Powered by AbleSci AI