The Impact of Modern Anti-Diabetic Treatment on Endothelial Progenitor Cells

Abstract

Diabetes is one of the leading chronic diseases globally with a significant impact on mortality. This condition is associated with chronic microvascular and macrovascular complications caused by vascular damage. Recently, endothelial progenitor cells (EPCs) raised interest due to their regenerative properties. EPCs are mononuclear cells that are derived from different tissues. Circulating EPCs contribute to regenerating the vessel’s intima and restoring vascular function. The ability of EPCs to repair vascular damage depends on their number and functionality. Diabetic patients have a decreased circulating EPC count and impaired EPC function. This may at least partially explain the increased risk of diabetic complications, including the increased cardiovascular risk in these patients. Recent studies have confirmed that many currently available drugs with proven cardiovascular benefits have beneficial effects on EPC count and function. Among these drugs are also medications used to treat different types of diabetes. This manuscript aims to critically review currently available evidence about the ways anti-diabetic treatment affects EPC biology and to provide a broader context considering cardiovascular complications. The therapies that will be discussed include lifestyle adjustments, metformin, sulphonylureas, gut glucosidase inhibitors, thiazolidinediones, dipeptidyl peptidase 4 inhibitors, glucagon-like peptide 1 receptor analogs, sodium-glucose transporter 2 inhibitors, and insulin.

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

“…For instance, isolated ECFCs from T2DM patients show impaired colony outgrowth, less tube formation, decreased proliferation, migration, and impaired in vivo neovascularization (the latter was shown in an animal model) [25,257]. Notably, improved glycemic control also positively impacts EPC numbers and improves the function of differentiated ECFCs [256,258]. Furthermore, the number of EPCs inversely correlates with body mass index (BMI) [259,260] and levels of insulin, leptin, and C-reactive protein (CRP) [260], with ECFCs originating from obese patients showing a slower proliferation rate [260].…”