Platelet activation in type 2 diabetes mellitus

P. Ferroni, S. Basili, A. Falco, Giovanni Davì

Research output: Contribution to journalArticle

289 Citations (Scopus)

Abstract

The abnormal metabolic state that accompanies diabetes renders arteries susceptible to atherosclerosis, being capable of altering the functional properties of multiple cell types, including endothelium and platelets. In particular, an altered platelet metabolism and changes in intraplatelet signaling pathways may contribute to the pathogenesis of atherothrombotic complications of diabetes. A variety of mechanisms may be responsible for enhanced platelet aggregation. Among them, hyperglycemia may represent a causal factor for in vivo platelet activation, and may be responsible for nonenzymatic glycation of platelet glycoproteins, causing changes in their structure and conformation, as well as alterations of membrane lipid dynamics. Furthermore, hyperglycemia-induced oxidative stress is responsible for enhanced peroxidation of arachidonic acid to form biologically active isoprostanes, which represents an important biochemical link between impaired glycemic control and persistent platelet activation. Finally, increased oxidative stress is responsible for activation of transcription factors and expression of redox-sensitive genes leading to a phenotypic switch of endothelium toward an adhesive, prothrombotic condition, initial platelet activation, adhesion and subsequent platelet aggregate formation. All this evidence is strengthened by the results of clinical trials documenting the beneficial effects of metabolic control on platelet function, and by the finding that aspirin treatment may even be more beneficial in diabetic than in high-risk non-diabetic patients. Attention to appropriate medical management of diabetic patients will have great impact on long-term outcome in this high-risk population.

Original languageEnglish
Pages (from-to)1282-1291
Number of pages10
JournalJournal of Thrombosis and Haemostasis
Volume2
Issue number8
DOIs
Publication statusPublished - Aug 2004

Fingerprint

Platelet Activation
Type 2 Diabetes Mellitus
Blood Platelets
Hyperglycemia
Endothelium
Oxidative Stress
Platelet Membrane Glycoproteins
Isoprostanes
Diabetes Complications
Membrane Lipids
Platelet Aggregation
Arachidonic Acid
Adhesives
Aspirin
Oxidation-Reduction
Atherosclerosis
Transcription Factors
Arteries
Clinical Trials
Population

Keywords

  • Atherosclerosis
  • Diabetes mellitus
  • Platelet activation

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Platelet activation in type 2 diabetes mellitus. / Ferroni, P.; Basili, S.; Falco, A.; Davì, Giovanni.

In: Journal of Thrombosis and Haemostasis, Vol. 2, No. 8, 08.2004, p. 1282-1291.

Research output: Contribution to journalArticle

Ferroni, P. ; Basili, S. ; Falco, A. ; Davì, Giovanni. / Platelet activation in type 2 diabetes mellitus. In: Journal of Thrombosis and Haemostasis. 2004 ; Vol. 2, No. 8. pp. 1282-1291.
@article{fe67ccdf646c4ebc90bb8b96eb7832e0,
title = "Platelet activation in type 2 diabetes mellitus",
abstract = "The abnormal metabolic state that accompanies diabetes renders arteries susceptible to atherosclerosis, being capable of altering the functional properties of multiple cell types, including endothelium and platelets. In particular, an altered platelet metabolism and changes in intraplatelet signaling pathways may contribute to the pathogenesis of atherothrombotic complications of diabetes. A variety of mechanisms may be responsible for enhanced platelet aggregation. Among them, hyperglycemia may represent a causal factor for in vivo platelet activation, and may be responsible for nonenzymatic glycation of platelet glycoproteins, causing changes in their structure and conformation, as well as alterations of membrane lipid dynamics. Furthermore, hyperglycemia-induced oxidative stress is responsible for enhanced peroxidation of arachidonic acid to form biologically active isoprostanes, which represents an important biochemical link between impaired glycemic control and persistent platelet activation. Finally, increased oxidative stress is responsible for activation of transcription factors and expression of redox-sensitive genes leading to a phenotypic switch of endothelium toward an adhesive, prothrombotic condition, initial platelet activation, adhesion and subsequent platelet aggregate formation. All this evidence is strengthened by the results of clinical trials documenting the beneficial effects of metabolic control on platelet function, and by the finding that aspirin treatment may even be more beneficial in diabetic than in high-risk non-diabetic patients. Attention to appropriate medical management of diabetic patients will have great impact on long-term outcome in this high-risk population.",
keywords = "Atherosclerosis, Diabetes mellitus, Platelet activation",
author = "P. Ferroni and S. Basili and A. Falco and Giovanni Dav{\`i}",
year = "2004",
month = "8",
doi = "10.1111/j.1538-7836.2004.00836.x",
language = "English",
volume = "2",
pages = "1282--1291",
journal = "Journal of Thrombosis and Haemostasis",
issn = "1538-7933",
publisher = "Wiley-Blackwell",
number = "8",

}

TY - JOUR

T1 - Platelet activation in type 2 diabetes mellitus

AU - Ferroni, P.

AU - Basili, S.

AU - Falco, A.

AU - Davì, Giovanni

PY - 2004/8

Y1 - 2004/8

N2 - The abnormal metabolic state that accompanies diabetes renders arteries susceptible to atherosclerosis, being capable of altering the functional properties of multiple cell types, including endothelium and platelets. In particular, an altered platelet metabolism and changes in intraplatelet signaling pathways may contribute to the pathogenesis of atherothrombotic complications of diabetes. A variety of mechanisms may be responsible for enhanced platelet aggregation. Among them, hyperglycemia may represent a causal factor for in vivo platelet activation, and may be responsible for nonenzymatic glycation of platelet glycoproteins, causing changes in their structure and conformation, as well as alterations of membrane lipid dynamics. Furthermore, hyperglycemia-induced oxidative stress is responsible for enhanced peroxidation of arachidonic acid to form biologically active isoprostanes, which represents an important biochemical link between impaired glycemic control and persistent platelet activation. Finally, increased oxidative stress is responsible for activation of transcription factors and expression of redox-sensitive genes leading to a phenotypic switch of endothelium toward an adhesive, prothrombotic condition, initial platelet activation, adhesion and subsequent platelet aggregate formation. All this evidence is strengthened by the results of clinical trials documenting the beneficial effects of metabolic control on platelet function, and by the finding that aspirin treatment may even be more beneficial in diabetic than in high-risk non-diabetic patients. Attention to appropriate medical management of diabetic patients will have great impact on long-term outcome in this high-risk population.

AB - The abnormal metabolic state that accompanies diabetes renders arteries susceptible to atherosclerosis, being capable of altering the functional properties of multiple cell types, including endothelium and platelets. In particular, an altered platelet metabolism and changes in intraplatelet signaling pathways may contribute to the pathogenesis of atherothrombotic complications of diabetes. A variety of mechanisms may be responsible for enhanced platelet aggregation. Among them, hyperglycemia may represent a causal factor for in vivo platelet activation, and may be responsible for nonenzymatic glycation of platelet glycoproteins, causing changes in their structure and conformation, as well as alterations of membrane lipid dynamics. Furthermore, hyperglycemia-induced oxidative stress is responsible for enhanced peroxidation of arachidonic acid to form biologically active isoprostanes, which represents an important biochemical link between impaired glycemic control and persistent platelet activation. Finally, increased oxidative stress is responsible for activation of transcription factors and expression of redox-sensitive genes leading to a phenotypic switch of endothelium toward an adhesive, prothrombotic condition, initial platelet activation, adhesion and subsequent platelet aggregate formation. All this evidence is strengthened by the results of clinical trials documenting the beneficial effects of metabolic control on platelet function, and by the finding that aspirin treatment may even be more beneficial in diabetic than in high-risk non-diabetic patients. Attention to appropriate medical management of diabetic patients will have great impact on long-term outcome in this high-risk population.

KW - Atherosclerosis

KW - Diabetes mellitus

KW - Platelet activation

UR - http://www.scopus.com/inward/record.url?scp=13244274961&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=13244274961&partnerID=8YFLogxK

U2 - 10.1111/j.1538-7836.2004.00836.x

DO - 10.1111/j.1538-7836.2004.00836.x

M3 - Article

C2 - 15304032

AN - SCOPUS:13244274961

VL - 2

SP - 1282

EP - 1291

JO - Journal of Thrombosis and Haemostasis

JF - Journal of Thrombosis and Haemostasis

SN - 1538-7933

IS - 8

ER -