Abstract
Diabetes mellitus is the fifth most common cause of death worldwide. Due to its chronic nature, diabetes is a debilitating disease for the patient and a relevant cost for the national health system. Type 2 diabetes mellitus is the most common form of diabetes mellitus (90% of cases) and is characteristically multifactorial, with both genetic and environmental causes. Diabetes patients display a significant increase in the risk of developing cardiovascular disease compared to the rest of the population. This is associated with increased blood clotting, which results in circulatory complications and vascular damage. Platelets are circulating cells within the vascular system that contribute to hemostasis. Their increased tendency to activate and form thrombi has been observed in diabetes mellitus patients (i.e., platelet hyperactivity). The oxidative damage of platelets and the function of pro-oxidant enzymes such as the NADPH oxidases appear central to diabetes-dependent platelet hyperactivity. In addition to platelet hyperactivity, endothelial cell damage and alterations of the coagulation response also participate in the vascular damage associated with diabetes. Here, we present an updated interpretation of the molecular mechanisms underlying vascular damage in diabetes, including current therapeutic options for its control.
Highlights
Diabetes mellitus (DM) is a heterogeneous metabolic disorder characterized by persistent hyperglycemia (HG), which can be diagnosed by quantifying glycated hemoglobin (HbA1c) in peripheral blood
Two main forms of DM are described: type 1, which is caused by genetic deficiency in insulin release, and type 2, which is caused by insulin resistance and has mixed genetic and lifestyle determinants
Since IGF1 has been described as a positive regulator of platelet signaling and responses [15], the upregulation of Insulin-like growth factor 1 receptor (IGF1R) is likely to contribute to platelet hyperactivity in T2DM
Summary
Diabetes mellitus (DM) is a heterogeneous metabolic disorder characterized by persistent hyperglycemia (HG), which can be diagnosed by quantifying glycated hemoglobin (HbA1c) in peripheral blood. Poor glycemic control in DM patients is accompanied by altered hematological parameters, such as hypercholesterolemia and dyslipidemia, and by a range of serious health complications, including cardiovascular diseases, nerve damage (neuropathy), kidney damage (nephropathy), eye damage (retinopathy), and limb and other peripheral tissue conditions. DM patients display a two- to fourfold increase in mortality caused by cardiovascular diseases as compared to the normal population [2]. Disturbed glycemic control increases the propensity for microvascular complications (e.g., retinopathy, neuropathy, and nephropathy) and contributes significantly to the risk factors for macrovascular events, such as age, physical activity, lifestyle, and ethnicity, leading to cardiovascular disease [4]. Men with diabetes have increased risk of developing cardiovascular diseases later in life (59–70 years) [5]. Blood hypercoagulability, reduced thrombolysis, and endothelial damage have all been reported and appear to contribute to vascular frailty in DM patients
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