Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue

Abstract

Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development.

Keywords: apoptosis; autophagy; diabetic cardiomyopathy; exosomes; ferroptosis; fibrosis; pyroptosis.

Figure 1

Diabetic cardiomyopathy mechanisms. Figure was generated using Servier Medical Art, provided by Servier, licensed under Creative Commons Attribution 3.0 Unported license.

Figure 2

The roles of organelle damage, oxidative stress, exosomes, epicardial adipose tissue (EAT) and activated fibroblasts in DCM. Epicardial adipose tissue (EAT). The figure was generated using Servier Medical Art, provided by Servier, licensed under Creative Commons Attribution 3.0 Unported license. Angiotensin II (Ang-II), matrix metalloproteases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), mitogen-activated protein kinase (MAPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), microRNA (miRNA).