Role of Endothelial Progenitor Cells in Vascular Dysfunction

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 September 2026 | Viewed by 1285

Editor


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Guest Editor
Department Woman-Mother-Child, Division of Pediatrics, DOHaD Laboratory, Lausanne University Hospital (CHUV), University of Lausanne (UNIL), Lausanne, Switzerland
Interests: cardiometabolic disorders; developmental programming; endothelial progenitor cells; oxidative stress; cellualr senescence; cellular therapy
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Dear Colleagues,

Cardiovascular disease (CVD) remains one of the leading causes of mortality worldwide, affecting populations in both developed and developing countries. Many forms of CVD, including atherosclerosis, arterial hypertension, and chronic heart failure, are closely associated with endothelial dysfunction, which reduces arterial elasticity and contributes to disease progression.

Endothelial progenitor cells (EPCs) are circulating components derived from the bone marrow that play a critical role in maintaining vascular integrity. Once mobilized, EPCs differentiate into mature endothelial cells and secrete various bioactive molecules and growth factors that support vasculogenesis and vascular homeostasis. EPCs can be classified based on their phenotype and in vivo function. Early EPCs, which are of hematopoietic origin, facilitate angiogenesis primarily through paracrine signaling but lack the ability to form mature endothelial cells. In contrast, late EPCs, also known as endothelial colony-forming cells (ECFCs), possess clonal potential and can proliferate, self-renew, migrate, differentiate, and promote vascular growth and neovascularization both in vitro and in vivo.

Reduced number and impaired function of EPCs are commonly observed in patients with CVD and may serve as predictive biomarkers for cardiovascular events. Dysfunctional EPCs have also been identified in individuals with low birth weight due to preterm birth or intrauterine growth restriction. Factors such as inflammation, oxidative stress, and cellular senescence negatively affect EPC function, whereas interventions such as statin therapy, antioxidant treatment, polyphenol intake, and physical exercise can enhance their activity. Given their regenerative potential, EPCs have recently been investigated for use in cell-based therapies for restoring endothelial integrity and promoting neovascularization in ischemic tissues across both animal models and clinical studies.

Dr. Catherine Yzydorczyk
Guest Editor

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Keywords

  • cardiovascular diseases
  • endothelial progenitor cells
  • vasculogenesis
  • angiogenesis
  • inflammation
  • oxidative stress
  • cellular senescence
  • developmental programming
  • cellular therapy

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Published Papers (1 paper)

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Research

27 pages, 12913 KB  
Article
Preserved Function of Endothelial Colony-Forming Cells in Female Rats with Intrauterine Growth Restriction: Protection Against Arterial Hypertension and Arterial Stiffness?
by Thea Chevalley, Floriane Bertholet, Marion Dübi, Maria Serena Merli, Mélanie Charmoy, Sybil Bron, Manon Allouche, Alexandre Sarre, Nicole Sekarski, Stéphanie Simoncini, Patrick Taffé, Umberto Simeoni and Catherine Yzydorczyk
Cells 2026, 15(2), 171; https://doi.org/10.3390/cells15020171 - 17 Jan 2026
Viewed by 983
Abstract
Individuals born after intrauterine growth restriction (IUGR) are at increased risk of long-term cardiovascular complications, including elevated blood pressure, endothelial dysfunction, and arterial stiffness. Endothelial progenitor cells (EPCs), particularly endothelial colony-forming cells (ECFCs), play a critical role in maintaining vascular homeostasis. Previously, Simoncini [...] Read more.
Individuals born after intrauterine growth restriction (IUGR) are at increased risk of long-term cardiovascular complications, including elevated blood pressure, endothelial dysfunction, and arterial stiffness. Endothelial progenitor cells (EPCs), particularly endothelial colony-forming cells (ECFCs), play a critical role in maintaining vascular homeostasis. Previously, Simoncini et al. observed that in a rat model of IUGR, six-month-old males exhibited elevated systolic blood pressure (SBP) and microvascular rarefaction compared with control (CTRL) rats. These vascular alterations were accompanied by reduced numbers and impaired function of bone marrow-derived ECFCs, which were associated with oxidative stress and stress-induced premature senescence (SIPS). In contrast, IUGR females of the same age and from the same litter did not exhibit higher SBP or microvascular rarefaction, raising the question of whether ECFC dysfunction in IUGR female rats can be present without vascular alterations. So, we investigated ECFCs isolated from six-month-old female IUGR offspring (maternal 9% casein diet) and CTRL females (23% casein diet). To complete the vascular assessment, we performed in vivo and in vitro investigations. No alteration in pulse wave velocity (measured by echo-Doppler) was observed; however, IUGR females showed decreased aortic collagen and increased elastin content compared with CTRL. Regarding ECFCs, those from IUGR females maintained their endothelial identity (CD31+/CD146+ ratio among viable CD45 cells) but exhibited slight alterations in progenitor marker expression (CD34) compared with those of CTRL females. Functionally, IUGR-ECFCs displayed a delayed proliferation phase between 6 and 24 h, while their ability to form capillary-like structures remained unchanged, however their capacity to form capillary-like structures was preserved. Regarding the nitric oxide (NO) pathway, a biologically relevant trend toward reduced NO levels and decreased endothelial nitric oxide synthase expression was observed, whereas oxidative stress and SIPS markers remained unchanged. Overall, these findings indicate that ECFCs from six-month-old female IUGR rats exhibit only minor functional alterations, which may contribute to vascular protection against increase SBP, microvascular rarefaction, and arterial stiffness. Full article
(This article belongs to the Special Issue Role of Endothelial Progenitor Cells in Vascular Dysfunction)
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