Does drug therapy reverse endothelial progenitor cell dysfunction in diabetes?

Research output: Contribution to journalReview article

27 Citations (Scopus)

Abstract

Endothelial progenitor cells (EPCs) are vital for the maintenance and repair of the endothelium. Decreased EPC number and function have been associated with increased cardiovascular (CVD) risk. Patients with diabetes have decreased number of circulating EPCs and decreased EPC function. This may account for some of the increased CVD risk seen in patients with diabetes that is not explained by traditional risk factors such as glycemic control, dyslipidemia and hypertension. Recent studies seem to indicate that drugs commonly used in diabetes patients such as metformin, thiazolidinediones, GLP-1 agonists, DPP-4 inhibitors, insulin, statins and ACE inhibitors may increase EPC number and improve EPC function. The mechanisms by which these drugs modulate EPC function may involve reduction in inflammation, oxidative stress and insulin resistance as well as an increase in nitric oxide (NO) bioavailability. This review will discuss the evidence in the literature regarding the above mentioned topics.

Original languageEnglish (US)
Pages (from-to)519-525
Number of pages7
JournalJournal of Diabetes and Its Complications
Volume27
Issue number5
DOIs
StatePublished - Sep 1 2013

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Drug Therapy
Cell Count
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Thiazolidinediones
Glucagon-Like Peptide 1
Metformin
Dyslipidemias
Endothelial Progenitor Cells
Angiotensin-Converting Enzyme Inhibitors
Pharmaceutical Preparations
Biological Availability
Endothelium
Insulin Resistance
Nitric Oxide
Oxidative Stress
Maintenance
Insulin
Hypertension
Inflammation

Keywords

  • Diabetes
  • Drug effect
  • Endothelial progenitor cell

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Does drug therapy reverse endothelial progenitor cell dysfunction in diabetes? / Desouza, Cyrus V.

In: Journal of Diabetes and Its Complications, Vol. 27, No. 5, 01.09.2013, p. 519-525.

Research output: Contribution to journalReview article

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