ArticleInternational journal of molecular sciences2018
Senescence Induces Dysfunctions in Endothelial Progenitor Cells and Osteoblasts by Interfering Translational Machinery and Bioenergetic Homeostasis.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Clozapine impairs angiogenic function and cellular bioenergetics in primary human endothelial progenitor cells and zebrafish: involvement of aryl hydrocarbon receptor signaling.Archives of toxicology · 2026Article
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Trimethylamine-N-Oxide Impedes Late Endothelial Progenitor Cell-Mediated Revascularization by Triggering Mitochondrial Apoptosis via Suppression of MnSOD.Cardiovascular therapeutics · 2025Article
- Senescence in the bone marrow microenvironment: A driver in development of therapy-related myeloid neoplasms.Journal of bone oncology · 2024Article
- Cryptocaryone induces apoptosis in human hepatocellular carcinoma cells by inhibiting aerobic glycolysis through Akt and c-Src signaling pathways.Journal of food and drug analysis · 2023Article
- Chemical Constituents and Anti-Angiogenic Principles from a Marine AlgicolousMolecules (Basel, Switzerland) · 2022Article
- ZnO Nanoparticles Induced Caspase-Dependent Apoptosis in Gingival Squamous Cell Carcinoma through Mitochondrial Dysfunction and p70S6K Signaling Pathway.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related bone diseases are partly caused by impaired bone integrity, which are closely related to osteoblasts’ activity and angiogenesis. Endothelial progenitor cells (EPCs) are the initiators of angiogenesis and found to have senescent-induced dysfunctions. The aim of this study is to investigate the effects of senescence in EPCs on osteogenesis and angiogenesis. Human primary EPCs and a murine osteoblast cell line (MC3T3-E1) are utilized in this study. The senescence of EPCs are induced by serial passages. When co-cultured with senescent EPCs, the osteoblasts demonstrate weakened alkaline phosphatase (ALP) activity and mineral deposition. On the other hand, osteoblast-induced migration decreases in senescent EPCs. As for the intracellular alterations of senescent EPCs, the activation of Akt/mTOR/p70S6K pathway, MnSOD and catalase are diminished. In contrast, the level of reactive oxygen species are significantly higher in senescent EPCs. Furthermore, senescent EPCs has decreased level intracellular ATP level and coupling efficiency for oxidative phosphorylation while the non-mitochondrial respiration and glycolysis are elevated. The senescence of EPCs impairs the functions of both osteoblasts and EPCs, suggesting EPCs’ role in the pathophysiology of age-related bone diseases. Targeting the alterations found in this study could be potential treatments.
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