Effects of emodin, a plant‐derived anthraquinone, on TGF‐β1‐induced cardiac fibroblast activation and function
| Autor: | Charity Fix, Mohamad Azhar, Mrinmay Chakrabarti, Daping Fan, Wayne Carver, Ethan Fix |
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| Rok vydání: | 2021 |
| Předmět: |
Male
0301 basic medicine Emodin Physiology Cardiac fibrosis p38 mitogen-activated protein kinases Clinical Biochemistry Smad2 Protein p38 Mitogen-Activated Protein Kinases Article Rats Sprague-Dawley Transforming Growth Factor beta1 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell Movement Fibrosis medicine Animals Smad3 Protein Fibroblast Cells Cultured Cell Proliferation Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 biology Myocardium Cell Biology Transforming growth factor beta Fibroblasts medicine.disease In vitro 030104 developmental biology medicine.anatomical_structure chemistry 030220 oncology & carcinogenesis biology.protein Cancer research Collagen Signal transduction Signal Transduction Transforming growth factor |
| Zdroj: | J Cell Physiol |
| ISSN: | 1097-4652 0021-9541 |
| Popis: | 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. 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 non-canonical (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. |
| Databáze: | OpenAIRE |
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