Autor: |
Shih-Yi Lee, Yueh-Hsiung Kuo, Chen-Xuan Du, Cheng-Wei Huang, Hui-Chun Ku |
Jazyk: |
angličtina |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
Biomedicine & Pharmacotherapy, Vol 162, Iss , Pp 114709- (2023) |
Druh dokumentu: |
article |
ISSN: |
0753-3322 |
DOI: |
10.1016/j.biopha.2023.114709 |
Popis: |
Differentiation of cardiac fibroblasts into myofibroblasts is a critical event in the progression of cardiac fibrosis that causes pathological cardiac remodeling. Cardiac fibrosis is a hallmark of heart disease and is associated with a stiff myocardium and heart failure. This study investigated the effect of caffeic acid ethanolamide (CAEA), a novel caffeic acid derivative, on cardiac remodeling. Angiotensin (Ang) II was used to induce cardiac remodeling both in cell and animal studies. Treating cardiac fibroblast with CAEA in Ang II-exposed cell cultures reduced the expression of fibrotic marker α-smooth muscle actin (α-SMA) and collagen and the production of superoxide, indicating that CAEA inhibited the differentiation of fibroblast into myofibroblast after Ang II exposure. CAEA protects against Ang II-induced cardiac fibrosis and dysfunction in vivo, characterized by the alleviation of collagen accumulation and the recovery of ejection fraction. In addition, CAEA decreased Ang II-induced transforming growth factor-β (TGF-β) expression and reduced NOX4 expression and oxidative stress in a SMAD-dependent pathway. CAEA participated in the regulation of Ang II-induced TGF-β/SMAD/NOX4 signaling to prevent the differentiation of fibroblast into myofibroblast and thus exerted a cardioprotective effect. Our data support the administration of CAEA as a viable method for preventing the progression of Ang II-induced cardiac remodeling. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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