Special Issue "Diabetic Cardiomyopathy: Biomolecular Mechanisms and Treatment"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (31 January 2020) | Viewed by 35946
Interests: neurological diseases; neurodegeneration; natural compounds; poliphenols; reactive oxygen species; apoptosis; autophagy; mitochondria; endoplasmic reticulum; blood brain barrier; endothelium involvement
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Type 2 diabetes (T2D) represents the major risk factor for developing myocardial dysfunction and, at the late stage, heart failure (HF). The occurrence of Diabetic Cardiomyopathy (DCM) seems to occur independently of coronary artery disease. Indeed, although the number of cases of myocardial infarction in the T2D population has been reduced by 25% over the last 10 years, the incidence of HF is continuously increasing, making it the most worrying diabetes complication. This strongly reinforces the urgent need for better characterization of pathophysiological mechanisms underlying DCM and for identifying innovative therapeutic interventions to prevent cardiac dysfunction in T2D patients. To this end, epidemiological, imaging, and animal studies have aimed to highlight the mechanisms involved in the development of diabetic cardiomyopathy. Epidemiological observations clearly show that hyperglycaemia correlates with severity of cardiac dysfunction and mortality in T2D patients. Both animal and cellular studies have demonstrated that, in the context of diabetes, the heart loses its ability to utilize glucose, therefore leading to glucose overload in cardiomyocytes that, in turn, promotes oxidative stress. This has been shown to reduce protective authophagy and to activate apoptosis, thus altering heart contractility, calcium signaling, and mitochondrial function, leading to fibrosis and compromised diastolic function. This seems to correlate with early changes in cardiomyocyte metabolic function, mostly occurring in the presence of microvascular complicances. On the other hand, although tight glycaemic control has failed to improve cardiac function in T2D patients, recent clinical trials have reported cardiovascular benefit with hypoglycaemic antidiabetic drugs of the SGLT2-inhibitor family. This Special Issue aims to cover some recent advances in basic science studies addressed to better characterize the pathophysiology of early stages of DCM. Moreover, the correlation between biomolecular changes occurring in T2D with recent advances in the development of better therapeutic interventions will be taken into account for identifying better solutions to prevent and treat HF associated to T2D.
Prof. Vincenzo Mollace
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- diabetes mellitus
- myocardial dysfunction
- microvascular coronary artery disease
- oxidative stress
- cardiomyocyte apoptosis
- food supplementation
- mitochondrial-targeted therapy