ArticleOxidative medicine and cellular longevity2022
Aging-Related Endothelial Progenitor Cell Dysfunction and Its Association with IL-17 and IL-23 in HFmrEF Patients.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Glucose and Lipid Metabolic Mechanisms in Vascular Aging and Related Therapeutic Strategies.Reviews in cardiovascular medicine · 2026Review
- Endothelial Progenitor Cells in Life, Pregnancy and Disease.Expert reviews in molecular medicine · 2025Review
- Exercise Training After Myocardial Infarction Enhances Endothelial Progenitor Cells Function via NRG-1 Signaling.Cardiovascular toxicology · 2025Article
- Role of serum cytokines in the prediction of heart failure in patients with coronary artery disease.ESC heart failure · 2023Article
- Role of Endothelial Progenitor Cells in Frailty.International journal of molecular sciences · 2023Review
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Authors and funding
10 authors.
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Abstract
Background: Aging is an independent risk factor for heart failure (HF), and endothelial progenitor cell (EPC) function decreases with aging. Here, we further investigated whether age has a detrimental effect on circulating EPC function in HF with mildly reduced ejection fraction (HFmrEF) and its relationship with systemic inflammation. Methods: 58 HFmrEF patients were recruited. The adhesive, migrative, and proliferative activities of circulating EPCs, MAGGIC scores, and plasma interleukin (IL)-17 and IL-23 levels of these patients were assessed. Results: Older patients with HFmrEF had higher MAGGIC scores and lower circulating EPC adhesion, migration, and proliferation than younger patients. The similar tendency was observed in plasma IL-17 and IL-23 levels. The EPC functions were negatively associated with MAGGIC scores and plasma IL-17 or IL-23 levels. Conclusions: In patients with HFmrEF, aging leads to attenuated circulating EPC function, which is correlated with disease severity and systemic inflammation. The present investigation provides some novel insights into the mechanism and intervention targets of HFmrEF.
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