Biomedical Letters

The role of TANK-binding kinase 1 (TBK1) and C-reactive protein in myocardial infarction inflammatory response

Abdlay Marty Lopes de Carvalho 1, Erica Audrey Limbenga 2, Genshan Ma 1*

1 Department of Cardiology, The Affiliated Zhongda Hospital of Southeast University, Dingjiaqiao, Nanjing 210009, China

2 Department of Neurology, The Affiliated Zhongda Hospital of Southeast University, Dingjiaqiao, Nanjing 210009, China

Abstract

The inflammatory response is an immunobiological defense mechanism triggered by damage to living tissues. Inflammation plays a crucial role in pathogenesis of atherosclerosis and vascular disease. Inflammatory response is the main player in the initiation and progression of atherosclerosis, which in turn leads to occlusion of coronary arteries inducing ischaemic events finally causing injury and consequent death of cardiomyocytes. Despite decades long improvements in diagnosing and treatment of coronary heart disease, questions about how to prevent and/or stop ventricular remodeling in post Myocardial infarction still rises. This paper discusses some recent findings and the role of some inflammatory biomarkers, namely C-reactive protein and TBK1 in Myocardial Infarction and their impact in post myocardial infarction ventricular remodeling due to prolonged inflammatory response. Deeper understanding the role of TBK1 in the inflammatory response post myocardial infarction could be of significant importance to the design of novel therapeutic strategies targeting the resolution of prolonged inflammatory response which takes place post myocardial infarction leading to ventricular remodeling and impaired ventricular function.

Key words: TANK-Binding Kinase 1 (TBK1), C-reactive protein, myocardial infarction, ventricular remodeling, cardiac remodeling, inflammation.

Received March 23, 2015 Revised April 02, 2015 Accepted April 05, 2015

*Correspondence: Genshan Ma Email: magenshan@hotmail.com.