Molecular mechanisms linking diabetes to the accelerated development of atherosclerosis.
Diabetes mellitus is a major independent risk factor for the development of cardiovascular disease, and both type 1 and type 2 diabetes have been shown to accelerate the development of atherosclerosis, the underlying cause of most myocardial infarctions. Despite the profound clinical importance of vascular disease in patients with diabetes mellitus, our understanding of the relative contributions of insulin resistance and hyperglycemia to atherogenesis is not complete. Furthermore, the molecular and cellular pathways that are involved in disease progression are not clear. In this review, we summarize our current understanding of the potential mechanisms that link diabetes to atherosclerosis and indicate existing gaps in our knowledge.
Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
Melec G
MG
Zeadin
Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada; Department of Chemistry and Chemical Biology McMaster University, Hamilton, Ontario, Canada.
Christina I
CI
Petlura
Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada; Department of Chemistry and Chemical Biology McMaster University, Hamilton, Ontario, Canada. Electronic address: Geoff.Werstuck@taari.ca.
Geoff H
GH
Werstuck
D050197:Atherosclerosis / Q000097:blood / Q000503:physiopathology* / Q000517:prevention & control; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D018450:Disease Progression; D004721:Endoplasmic Reticulum / Q000378:metabolism; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D018384:Oxidative Stress; D012307:Risk Factors; D015398:Signal Transduction
atherosclerosis; athérosclérose; diabetes; diabète; hyperglycemia; hyperglycémie; insulin resistance; insulinorésistance; molecular mechanisms; mécanismes moléculaires