IMR Press / FBS / Volume 4 / Issue 3 / DOI: 10.2741/S308

Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Insulin resistance, metabolic stress, and atherosclerosis
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1 Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA, 19140
2 Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, 19140
3 Thrombosis Research Center of Temple University School of Medicine, Philadelphia, PA, 19140
4 School of Pharmaceutical Science, Zhejiang University of Technology, Hangzhou, 310014, PR, China

*Author to whom correspondence should be addressed.

Academic Editor: Xiao-Feng Yang

Front. Biosci. (Schol Ed) 2012, 4(3), 916–931;
Published: 1 January 2012
(This article belongs to the Special Issue Amylin in vasodilation, energy expenditure and inflammation)

Atherosclerosis, a pathological process that underlies the development of cardiovascular disease, is the primary cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). T2DM is characterized by hyperglycemia and insulin resistance (IR), in which target tissues fail to respond to insulin. Systemic IR is associated with impaired insulin signaling in the metabolic tissues and vasculature. Insulin receptor is highly expressed in the liver, muscle, pancreas, and adipose tissue. It is also expressed in vascular cells. It has been suggested that insulin signaling in vascular cells regulates cell proliferation and vascular function. In this review, we discuss the association between IR, metabolic stress, and atherosclerosis with focus on 1) tissue and cell distribution of insulin receptor and its differential signaling transduction and 2) potential mechanism of insulin signaling impairment and its role in the development of atherosclerosis and vascular function in metabolic disorders including hyperglycemia, hypertension, dyslipidemia, and hyperhomocysteinemia. We propose that insulin signaling impairment is the foremost biochemical mechanism underlying increased cardiovascular morbidity and mortality in atherosclerosis, T2DM, and metabolic syndrome.

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