Diabetic Cardiomyopathy: Role of Cell Death, Exosomes, Fibrosis and Epicardial Adipose Tissue.
Antonella GaleoneAlessia AnnicchiaricoCinzia BuccolieroBarbara BarileGiovanni Battista LucianiFrancesco OnoratiGrazia Paola NicchiaGiacomina BrunettiPublished in: International journal of molecular sciences (2024)
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.
Keyphrases
- heart failure
- left ventricular
- cell death
- angiotensin ii
- oxidative stress
- adipose tissue
- type diabetes
- cell cycle arrest
- cardiac resynchronization therapy
- endoplasmic reticulum stress
- hypertrophic cardiomyopathy
- acute heart failure
- blood pressure
- insulin resistance
- angiotensin converting enzyme
- cardiovascular disease
- vascular smooth muscle cells
- mitral valve
- left atrial
- aortic stenosis
- working memory
- atrial fibrillation
- signaling pathway
- wound healing
- glycemic control
- nlrp inflammasome
- liver fibrosis
- ejection fraction