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Published on: April 1, 2015
Diabetes mellitus and thrombosis
Natale Vazzana1, Paola Ranalli, Chiara Cuccurullo
1Internal Medicine and Center of Excellence on Aging, G. D'Annunzio University Foundation, Chieti, Italy.
Insights
Patients with diabetes mellitus face accelerated atherothrombosis due to prothrombotic factors. Diabetic platelets exhibit dysregulated signaling, leading to increased adhesion and aggregation, driven by hyperglycemia and inflammation.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Hematology
Background:
- Atherothrombosis is a primary cause of death in diabetes mellitus patients.
- Diabetic patients exhibit a prothrombotic state involving endothelial dysfunction, coagulation activation, and platelet hyper-reactivity.
Purpose of the Study:
- To review the mechanisms underlying accelerated atherothrombosis in diabetes mellitus.
- To provide an overview of current knowledge on diabetic prothrombotic mechanisms.
Main Methods:
- Literature review of studies on diabetes mellitus and atherothrombosis.
- Analysis of mechanisms including platelet signaling, hyperglycemia, insulin resistance, inflammation, and oxidative stress.
Main Results:
- Diabetic platelets show dysregulated signaling pathways.
- Enhanced platelet adhesion, activation, and aggregation are observed in diabetic patients.
- Hyperglycemia, insulin resistance, inflammation, and oxidative stress contribute to these alterations.
Conclusions:
- Understanding these mechanisms is crucial for managing atherothrombosis risk in diabetes.
- Diabetic prothrombotic state is multifactorial, involving complex interactions.
Abstract:
Atherothrombosis is the leading cause of morbidity and mortality in patients with diabetes mellitus. Several mechanisms contribute to the diabetic prothrombotic state, including endothelial dysfunction, coagulative activation and platelet hyper-reactivity. In particular, diabetic platelets are characterised by dysregulation of several signaling pathways leading to enhanced adhesion, activation and aggregation. These alterations result from the interaction among hyperglycemia, insulin resistance, inflammation and oxidative stress. This review will provide an overview of the current status of knowledge on mechanisms of accelerated atherothrombosis in patients with diabetes mellitus.
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