Journals / Marmara Medical Journal / 2026 / Volume: 39 Issue: 1

Angiotensin-(1-7) counteracts Angiotensin II-induced senescence in telomerase-immortalized human mesenchymal stem cells

Asmaa Abuaisha(NEAR EAST UNIVERSITY)0000-0003-2869-6620
Merdiye Maviş(Near East University)0000-0002-5493-4568
Ibrahim Benter(International University)0000-0001-5045-368X
Nedime Serakinci(Cyprus International University)0000-0002-1884-0839
Pages
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Publication Date
2026-01-28
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Ang-(1-7) attenuates AngII-induced cellular senescence and improves proliferative potential in hMSCs-telo1 cells, suggesting a modulatory role in stress-induced senescence and potential relevance for stem cell-based therapies.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Angiotensin-(1-7) (Ang-(1-7)) exerts protective and anti-inflammatory effects, whereas angiotensin II (AngII) promotes pro-inflammatory and pro-oxidative processes.
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Key Findings & Data:This study aimed to evaluate the potential inhibitory role of Ang-(1-7) in AngII-induced senescence in telomerase-immortalized human mesenchymal stem cells (hMSCs-telo1).
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Conclusion & Impact:Conclusion: Ang-(1-7) attenuates AngII-induced cellular senescence and improves proliferative potential in hMSCs-telo1 cells, suggesting a modulatory role in stress-induced senescence and potential relevance for stem cell-based therapies.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Angiotensin-(1-7) · Angiotensin II · Cellular senescence

Abstract

Objective: Angiotensin-(1-7) (Ang-(1-7)) exerts protective and anti-inflammatory effects, whereas angiotensin II (AngII) promotes pro-inflammatory and pro-oxidative processes. Cellular senescence is an irreversible cell cycle arrest that can be induced in vitro by a variety of cellular stresses, including AngII “stress-induced premature senescence (SIPS)”. This study aimed to evaluate the potential inhibitory role of Ang-(1-7) in AngII-induced senescence in telomerase-immortalized human mesenchymal stem cells (hMSCs-telo1). Materials and Methods: Senescence was induced using AngII at various time points and concentrations. Based on preliminary optimization experiments, cells were treated with AngII (10-⁶ M) for 48 hours, followed by Ang-(1-7) treatment (10-⁶ M) for an additional 24 hours. Following treatments, cellular senescence and functional responses were assessed using proliferation analysis based on population doubling levels (PDLs), senescence associated-beta-galactosidase (SA-β-gal) staining, and colony forming unit (CFU) assays. Results: No marked morphological differences were observed among the experimental groups. However, Ang-(1-7) treatment significantly reduced the proportion of SA-β-gal-positive cells in AngII-induced senescent hMSCs-telo1, showing a 1.65-fold decrease. In parallel, Ang-(1-7) partially restored cell proliferation capacity. Conclusion: Ang-(1-7) attenuates AngII-induced cellular senescence and improves proliferative potential in hMSCs-telo1 cells, suggesting a modulatory role in stress-induced senescence and potential relevance for stem cell-based therapies.

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Cite This Article

Abuaisha, A., Maviş, M., Emiroğlu, S., Benter, I., Serakinci, N. (2026). Angiotensin-(1-7) counteracts Angiotensin II-induced senescence in telomerase-immortalized human mesenchymal stem cells. Marmara Medical Journal, Volume: 39 Issue: 1. https://doi.org/10.5472/marumj.1873490

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