Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells
Azra Kulovic-Sissawo,
Carolina Tocantins,
Mariana S. Diniz,
Elisa Weiss,
Andreas Steiner,
Silvija Tokic,
Corina T. Madreiter-Sokolowski,
Susana P. Pereira,
Ursula Hiden
Affiliations
Azra Kulovic-Sissawo
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Carolina Tocantins
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Mariana S. Diniz
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Elisa Weiss
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Andreas Steiner
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Silvija Tokic
Research Unit of Analytical Mass Spectrometry, Cell Biology and Biochemistry of Inborn Errors of Metabolism, Department of Paediatrics and Adolescent Medicine, Medical University of Graz, Auenbruggerplatz 34, 8036 Graz, Austria
Corina T. Madreiter-Sokolowski
Division of Molecular Biology and Biochemistry, Medical University of Graz, Neue Stiftingtalstraße 6, 8010 Graz, Austria
Susana P. Pereira
CNC-UC—Center for Neuroscience and Cell Biology, University of Coimbra, Rua Larga, 3004-504 Coimbra, Portugal
Ursula Hiden
Perinatal Research Laboratory, Department of Obstetrics and Gynaecology, Medical University of Graz, Auenbruggerplatz 14, 8036 Graz, Austria
Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.
