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The impact of insulin resistance on endothelial function, progenitor cells and repair

The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

Adil Rajwani

The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

Stephen B Wheatcroft

The Academic Unit of Cardiovascular Medicine, The LIGHT Laboratories, University of Leeds, Clarendon Way, Leeds, LS2 9JT, UK.

The structural and functional integrity of the vascular endothelium plays a critical role in vascular homeo-stasis. Insulin resistance, an important risk factor for cardiovascular disease, is thought to promote atherosclerosis through a reciprocal relationship with endothelial dysfunction. In health, cumulative damage to endothelial cells incurred by exposure to risk factors is mitigated by endogenous reparative processes. Disruption of the balance between endothelial damage and repair may mediate atherosclerotic progression. Bone marrow-derived ‘endothelial progenitor cells' (EPC) have been identified as significant contributors to endogenous vascular repair. Insulin resistance is associated with a spectrum of biochemical abnormalities which have the potential to reduce the availability of EPCs and diminish their capacity for vascular repair. Many lifestyle and pharmacological interventions which improve insulin resistance also increase the numbers and functionality of EPCs. Cell-based therapies may also hold promise for the prevention and treatment of cardiovascular disease.

Key Words: diabetes mellitus • insulin resistance • endothelial dysfunction • endothelial progenitor cells

Diabetes and Vascular Disease Research, Vol. 4, No. 2, 103-111 (2007)
DOI: 10.3132/dvdr.2007.027


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