The Potential Role of Interleukin-37 in Diabetic Cardiomyopathy

Abstract

Cardiovascular disease is the major reason of death in patients with Type 2 diabetes mellitus (T2DM) and accounts for up to 80% of associated mortality [1]. Diabetic cardiomyopathy (DCM), initially reported by Rubler and colleagues from diabetic patients who died of heart failure without cardiovascular disease in 1972, is characterized by lipid accumulation in cardiomyocytes, fetal gene reactivation, and cardiac hypertrophy, which together confers a 2-3 fold increased risk of heart failure [2,3]. The pathophysiological mechanisms underlying the characteristic features of diabetic cardiomyopathy are poorly understood, although multiple factors including hyperglycemia, hyperinsulinemia and hyperlipidemia mediated lipid accumulation, apoptosis, ROS stress, inflammation, as well as fibrosis, remodeling of cardiomyocytes are implicated [4]. IL-37 plays an important role in both innate and adaptive immunity, which has been reported to be associated with various kinds of inflammatory and autoimmune diseases [5,6]. Recent studies also showed that IL-37 played a role in tumorigenesis, angiogenesis, furthermore in autophagy and insulin sensitivity [7-10]. In this paper, we mainly point out the widespread potentially regulatory functions of IL-37 in DCM.