| Title: |
Dynamic Changes in Circulating Osteogenic Progenitor Cells Following TAVI: Implications for Vascular Remodeling—EPC and EPC-OCN Dynamics After TAVI |
| Authors: |
Lia Schoenfeld; Pablo Codner; Merry Abitbol; Ben Cohen; Dorit Leshem Lev; Amos Levi; Ariel Nakache; Guy Witberg; Yeela Talmor Barkan; Ran Kornowski; Leor Perl |
| Source: |
Journal of Clinical Medicine ; Volume 15 ; Issue 7 ; Pages: 2752 |
| Publisher Information: |
Multidisciplinary Digital Publishing Institute |
| Publication Year: |
2026 |
| Collection: |
MDPI Open Access Publishing |
| Subject Terms: |
aortic stenosis; endothelial progenitor cells; osteocalcin; transcatheter aortic valve implantation; vascular calcification |
| Description: |
Background: The prevalence of severe aortic stenosis (AS) is increasing, in accordance with a longer life expectancy. Aortic valve calcification is a multifactorial pathological process involving a complex interplay between different types of regenerative cellular and genetic factors. Among these cells, endothelial progenitor cells (EPCs) and their osteoblastic phenotype subpopulation (EPC-OCNs) have been implicated in vascular remodeling and disease progression. Objectives: To assess longitudinal changes in EPC and EPC-OCN levels in patients with severe symptomatic AS undergoing transcatheter aortic valve implantation (TAVI). Methods: In this prospective observational study, 65 patients with severe AS undergoing TAVI were enrolled. Circulating EPC and EPC-OCN levels were quantified by flow cytometry before the procedure, at 4 ± 1 days, and at 90 ± 29 days after TAVI. EPCs were defined by expression of CD133, CD34, and VEGFR-2. Results: Circulating EPC levels remained unchanged throughout the follow-up. In contrast, circulating EPC-OCNs increased significantly over time. Specifically, CD133+/VEGFR-2+/OCN+ cells rose from 2.50% to 6.25%, CD34+/VEGFR-2+/OCN+ from 2.04% to 4.05%, and VEGFR-2+/OCN+ from 1.46% to 3.01% (all p < 0.01). This suggests an osteogenic response to TAVI, while classical endothelial repair mechanisms were not systemically activated. Conclusions: EPC-OCNs increased significantly following TAVI, possibly reflecting ongoing tissue remodeling or calcification processes. In contrast, the stability of classical EPCs levels suggests limited systemic endothelial regeneration. These observations underscore the potential role of EPC-OCNs as markers or modulators of pre- and post-TAVI vascular remodeling. |
| Document Type: |
text |
| File Description: |
application/pdf |
| Language: |
English |
| Relation: |
Cardiovascular Medicine; https://dx.doi.org/10.3390/jcm15072752 |
| DOI: |
10.3390/jcm15072752 |
| Availability: |
https://doi.org/10.3390/jcm15072752 |
| Rights: |
https://creativecommons.org/licenses/by/4.0/ |
| Accession Number: |
edsbas.905FCB1F |
| Database: |
BASE |