MicroRNA-21 prevents excessive inflammation and cardiac dysfunction after myocardial infarction through targeting KBTBD7

• Published in: Cell death & disease Vol. 9; no. 7; pp. 769 - 14
• Main Authors: Yang, Linshan, Wang, Bo, Zhou, Qingqing, Wang, Yiru, Liu, Xingguang, Liu, Zhongmin, Zhan, Zhenzhen
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 10.07.2018; Springer Nature B.V
• Subjects: 13/1; 13/109; 13/21; 13/51; 13/89; 13/95; 14/19; 14/34; 64/60; Antibodies; Biochemistry; Biomedical and Life Sciences; Cardiovascular diseases; CD11b antigen; Cell activation; Cell Biology; Cell Culture; Coronary artery; Coronary artery disease; Cytokines; Heart attacks; Heat shock proteins; High mobility group proteins; HMGB1 protein; Hsp60 protein; Immunology; Inflammation; Interleukin 6; Life Sciences; Macrophages; MicroRNAs; miRNA; Monocytes; Myocardial infarction; NF-κB protein; Rodents; Therapeutic applications; Tumor necrosis factor-α

The excessive inflammation triggered by damage-associated molecular patterns (DAMPs) after myocardial infarction (MI) is responsible for the development of cardiac dysfunction and adverse remodeling, while the mechanisms by which inflammation is fine tuned remain to be fully elucidated. MicroRNA-21...