Impact of myeloid differentiation protein 1 on cardiovascular disease

Cardiovascular disease remains the leading cause of disability and mortality worldwide and a significant global burden. Many lines of evidence suggest complex remodeling responses to cardiovascular disease, such as myocardial ischemia, hypertension and valve disease, which lead to poor clinical outcomes, including heart failure, arrhythmia and sudden cardiac death (SCD). The mechanisms underlying cardiac remodeling are closely related to reactive oxygen species (ROS) and inflammation. Myeloid differentiation protein 1 (MD1) is a secreted glycoprotein known as lymphocyte antigen 86. The complex of MD1 and radioprotective 105 (RP105) is an important regulator of inflammation and is involved in the modulation of vascular remodeling and atherosclerotic plaque development. A recent study suggested that the expression of MD1 in hypertrophic cardiomyopathy (HCM) patients is decreased compared with that in donor hearts. Therefore, MD1 may play an important role in the pathological processes of cardiovascular disease and have potential clinical value. Here, this review aims to discuss the current knowledge regarding the role of MD1 in the regulation of cardiac pathophysiology.