Background: Endothelial progenitor cells (EPCs) have an important role in repair following vascular injury. Telomere length has been shown to be correlated with genome stability and overall cell health. We hypothesized that both EPCs and telomere size are related to protective mechanisms against coronary artery disease. Our aim was to evaluate the level and function of circulating EPCs and telomere length in patients with multiple cardiovascular risk factors and anatomically normal coronary arteries vs. matched controls.
Methods: We included 24 patients, with coronary CTA demonstrating normal coronaries and a high risk of CAD of >10% by ASCVD risk estimator. Control groups included 17 patients with similar cardiovascular profiles but with established CAD and a group of 20 healthy volunteers. Circulating EPCs levels were assessed by flow cytometry for expression of vascular endothelial growth factor receptor 2, CD34 and CD133. The capacity of the cells to form colony forming units (CFUs) was quantified after 1 week of culture. Telomere length was determined by the southern blotting technique.
Results: Patients with high risk for CVD and normal coronaries had augmented EPCs function, compared with the CAD group (1.1 vs. 0.22 CFU/f; P = 0.04) and longer telomeres compared with the CAD group (10.7 kb vs. 2.8 kb P = 0.015). These patients displayed a similar profile to the healthy group.
Conclusion: Patients with a high risk for CAD, but normal coronary arteries have EPCs function and telomere length which resemble healthy volunteers, and augmented compared with patients with established CAD, which could serve as a protective mechanism against atherosclerosis development in these high-risk patients.
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http://dx.doi.org/10.1097/MCA.0000000000001174 | DOI Listing |
Alzheimers Dement
December 2024
Institute of Public and Preventative Health, Augusta, GA, USA.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of São Paulo Universidade de São Paulo, São Paulo, Brazil.
Background: The Down Syndrome (DS), also referred to as trisomy of chromosome 21, is a prevalent cause of intellectual disability and also contributes to the acceleration of aging, among other developmental and health concerns. Certain pathological characteristics shared by DS and Alzheimer's Disease (AD) indicate similar commonalities. This study aims to unravel the relationship between the canonical Wnt/pathway, the amyloid precursor protein processing, the telomere shortening in DS individuals.
View Article and Find Full Text PDFBackground: People living with dementia (PWD) have upregulated inflammatory pathways, exaggerated metabolic aging, and cellular aging. They also have declines in physical function and heightened fall-risk. Understanding the physiologic factors that influence physical decline and fall-risk in PWD is vital to assess and prevent adverse health outcomes, such as future falls.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.
Background: Leukocyte telomere length (LTL) serves as a proxy for tissue-specific TL and peripheral immune aging. Its association with aging-related brain endophenotypes, cognitive functioning, and Alzheimer's disease (AD) risk is established, but the underlying molecular mechanisms remain elusive. Investigating LTL's association with AD biomarkers is crucial for identifying its role in brain resilience and disease progression.
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