“Diabetic platelets” are characterized by dysregulation of several signaling pathways leading to persistent in vivo platelet activation, induced by hyperglycemia, insulin resistance, inflammation, oxidative stress, and endothelial dysfunction. Both antihyperglycemic drugs, addressing the upward metabolic abnormalities, and antiplatelet agents, directly targeting the diabetic platelet, have the potential to curb persistent platelet activation in this setting. The pathophysiological evidence of enhanced platelet hyperreactivity/activation in DM, coupled with the epidemiological evidence of suboptimal response to aspirin in this setting, as it emerged in metanalyses of clinical trials, raised the hypothesis of an “interindividual variability” in the response to aspirin. Future efforts to decrease the thrombotic burden in diabetes should target specific disease-based mechanisms, including enhanced platelet turnover. Availability of high-throughput techniques open a novel perspective, with a deeper insight on transcriptomics and posttranscriptional regulation of platelets. Both platelet miRNAs and platelet-derived microparticles might not only reflect but also affect platelet function, and that of other cells, and may represent potentially useful biomarkers of platelet hyperreactivity and antiplatelet drug response.

The Role of Platelets in Diabetes Mellitus

Santilli, Francesca
;
Simeone, Paola;Liani, Rossella
2019

Abstract

“Diabetic platelets” are characterized by dysregulation of several signaling pathways leading to persistent in vivo platelet activation, induced by hyperglycemia, insulin resistance, inflammation, oxidative stress, and endothelial dysfunction. Both antihyperglycemic drugs, addressing the upward metabolic abnormalities, and antiplatelet agents, directly targeting the diabetic platelet, have the potential to curb persistent platelet activation in this setting. The pathophysiological evidence of enhanced platelet hyperreactivity/activation in DM, coupled with the epidemiological evidence of suboptimal response to aspirin in this setting, as it emerged in metanalyses of clinical trials, raised the hypothesis of an “interindividual variability” in the response to aspirin. Future efforts to decrease the thrombotic burden in diabetes should target specific disease-based mechanisms, including enhanced platelet turnover. Availability of high-throughput techniques open a novel perspective, with a deeper insight on transcriptomics and posttranscriptional regulation of platelets. Both platelet miRNAs and platelet-derived microparticles might not only reflect but also affect platelet function, and that of other cells, and may represent potentially useful biomarkers of platelet hyperreactivity and antiplatelet drug response.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11564/706135
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