ArticleInternational journal of molecular medicine2018
Nrf2 protects against diabetic dysfunction of endothelial progenitor cells via regulating cell senescence.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- Quercetin Mitigates Oxidative Stress-Induced Premature Senescence in SH-SY5Y Neuronal-like Cells.International journal of molecular sciences · 2026Article
- Update on the correlation between mitochondrial function and osteonecrosis of the femoral head osteocytes.Redox report : communications in free radical research · 2025Review
- Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2.Biomolecules · 2025Review
- The NRF2/ID2 Axis in Vascular Smooth Muscle Cells: Novel Insights into the Interplay between Vascular Calcification and Aging.Aging and disease · 2024Article
- Nrf2 activation: a key mechanism in stem cell exosomes-mediated therapies.Cellular & molecular biology letters · 2024Review
- Article
- Targeting the redox system for cardiovascular regeneration in aging.Aging cell · 2023Review
- Sodium tanshinone IIA sulfonate ameliorates neointima by protecting endothelial progenitor cells in diabetic mice.BMC cardiovascular disorders · 2023Article
- Vascular Ageing: Mechanisms, Risk Factors, and Treatment Strategies.International journal of molecular sciences · 2023Review
- Implications of Senescent Cell Burden and NRF2 Pathway in Uremic Calcification: A Translational Study.Cells · 2023Article
- Molecular Mechanism of Fucoidan Nanoparticles as Protector on Endothelial Cell Dysfunction in Diabetic Rats' Aortas.Nutrients · 2023Article
- Efficacy of the monocarbonyl curcumin analog C66 in the reduction of diabetes-associated cardiovascular and kidney complications.Molecular medicine (Cambridge, Mass.) · 2022Review
- Pharmaceutical Activation of Nrf2 Accelerates Diabetic Wound Healing by Exosomes from Bone Marrow Mesenchymal Stem Cells.International journal of stem cells · 2022Article
- Regulation of endothelial progenitor cell functions during hyperglycemia: new therapeutic targets in diabetic wound healing.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Protective Effects of Curcumin in Cardiovascular Diseases-Impact on Oxidative Stress and Mitochondria.Cells · 2022Review
- Notoginsenoside R1 alleviates high glucose-induced inflammation and oxidative stress in HUVECs via upregulating miR-147a.The Kaohsiung journal of medical sciences · 2021Article
- Harnessing the cardiovascular benefits of exercise: Are Nrf2 activators useful?Sports medicine and health science · 2021Review
- Upregulating CXCR7 accelerates endothelial progenitor cell-mediated endothelial repair by activating Akt/Keap-1/Nrf2 signaling in diabetes mellitus.Stem cell research & therapy · 2021Article
- Regulatory Role of Nrf2 Signaling Pathway in Wound Healing Process.Molecules (Basel, Switzerland) · 2021Review
- Role of Nrf2 in cell senescence regulation.Molecular and cellular biochemistry · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes is associated with an increased risk of cardiovascular disease. A decrease in the number and functionality of endothelial progenitor cells (EPCs) leads to reduced endothelial repair and the development of cardiovascular disease. The aim of the present study was to explore the effect and underlying mechanisms of nuclear factor erythroid 2‑related factor 2 (Nrf2) on EPC dysfunction caused by diabetic mellitus. The biological functions of EPCs in streptozotocin‑induced diabetic mice were evaluated, including migration, proliferation, angiogenesis and the secretion of vascular endothelial growth factor (VEGF), stromal‑derived growth factor (SDF) and nitric oxide (NO). Oxidative stress levels in diabetic EPCs were also assessed by detecting intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA). EPC senescence was evaluated by measuring p16 and b‑gal expression and observing the senescence‑associated secretory phenotype. In addition, the function of EPCs and level of oxidative stress were assessed following Nrf2 silencing or activation. Nrf2 silencing resulted in a decrease of EPC biological functions, accelerated cell senescence and increased oxidative stress, as indicated by ROS and MDA upregulation accompanied with decreased SOD activity. Furthermore, Nrf2 silencing inhibited migration, proliferation and secretion in EPCs, while it increased oxidative stress and cell senescence. Nrf2 activation protected diabetic EPCs against the effects of oxidative stress and cell senescence, ameliorating the biological dysfunction of EPCs derived from mice with diabetes. In conclusion, Nrf2 overexpression protected against oxidative stress‑induced functional damage in EPCs derived from diabetic mice by regulating cell senescence.
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