Downregulation of interferon-induced protein with tetratricopeptide repeats 3 relieves the inflammatory response and myocardial fibrosis of mice with myocardial infarction and improves their cardiac function
Author:
Affiliation:
1. Department of Internal Medicine, Hebei Medical University, No. 361, Zhongshan East Road, Chang’an District, Shijiazhuang, Hebei Province 050017, P.R. China
Publisher
Japanese Association for Laboratory Animal Science
Subject
General Veterinary,General Biochemistry, Genetics and Molecular Biology,Animal Science and Zoology,General Medicine
Link
https://www.jstage.jst.go.jp/article/expanim/70/4/70_21-0060/_pdf
Reference46 articles.
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2. 2. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990; 81: 1161–1172.
3. 3. Prabhu SD, Frangogiannis NG. The biological basis for cardiac repair after myocardial infarction: from inflammation to fibrosis. Circ Res. 2016; 119: 91–112.
4. 4. de Veer MJ, Sim H, Whisstock JC, Devenish RJ, Ralph SJ. IFI60/ISG60/IFIT4, a new member of the human IFI54/IFIT2 family of interferon-stimulated genes. Genomics. 1998; 54: 267–277.
5. 5. Johnson B, VanBlargan LA, Xu W, White JP, Shan C, Shi PY, et al. Human IFIT3 Modulates IFIT1 RNA binding specificity and protein stability. Immunity. 2018; 48: 487–499.e5.
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