Aspirin Reduces Cardiac Interstitial Fibrosis by Inhibiting Erk1/2-Serpine2 and P-Akt Signalling Pathways

• Published in: Cellular physiology and biochemistry Vol. 45; no. 5; pp. 1955 - 1965
• Main Authors: Li, Xuelian, Wang, GuoYuan, QiLi, MuGe, Liang, HaiHai, Li, TianShi, E, XiaoQiang, Feng, Ying, Zhang, Ying, Liu, Xiao, Qian, Ming, Xu, BoZhi, Shen, ZhiHang, Gitau, Samuel Chege, Zhao, DanDan, Shan, HongLi
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.03.2018; Cell Physiol Biochem Press GmbH & Co KG
• Subjects: Actins - metabolism; Akt; Angiotensin II - pharmacology; Animals; Aspirin; Aspirin - pharmacology; Aspirin - therapeutic use; beta Catenin - metabolism; Blood platelets; Cancer; Cardiac Fibrosis; Cardiovascular disease; Cell Line; Collagen; Collagen Type I - metabolism; Disease Models, Animal; Disease prevention; Erk1/2; Fibroblasts; Fibroblasts - cytology; Fibroblasts - drug effects; Fibroblasts - metabolism; Fibrosis; Growth factors; Heart Failure - metabolism; Heart Failure - pathology; Heart Failure - prevention & control; Kinases; Laboratory animals; Male; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinase 1 - metabolism; Mitogen-Activated Protein Kinase 3 - metabolism; Myocardium - cytology; Original Paper; Phosphorylation - drug effects; Proto-Oncogene Proteins c-akt - metabolism; Rodents; Serpin E2 - metabolism; SerpinE2; Signal Transduction - drug effects; Thrombosis; United States > US; Erk1/2; SerpinE2; Aspirin; Akt; Cardiac Fibrosis

Background/Aims: Cardiac interstitial fibrosis is an abnormality of various cardiovascular diseases, including myocardial infarction, hypertrophy, and atrial fibrillation, and it can ultimately lead to heart failure. However, there is a lack of practical therapeutic approaches to treat fibrosis and...