Placenta-Derived Mesenchymal Stem Cells in Chronic Kidney Disease via NADPH Oxidase
Journal of Clinical Medicine of Kazakhstan, cilt.23, sa.4, ss.25-32, 2026 (Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 23 Sayı: 4
- Basım Tarihi: 2026
- Doi Numarası: 10.23950/jcmk/19035
- Dergi Adı: Journal of Clinical Medicine of Kazakhstan
- Derginin Tarandığı İndeksler: Scopus
- Sayfa Sayıları: ss.25-32
- Anahtar Kelimeler: chronic kidney disease, mesenchymal stem cells, NADPH oxidase 4, oxidative stress, renal fibrosis
- Akdeniz Üniversitesi Adresli: Evet
Özet
Introduction: Chronic kidney disease (CKD) is associated with gradual deterioration of renal structure and function, accompanied by persistent fibrosis and oxidative imbalance. Excessive generation of reactive oxygen species (ROS), particularly through NADPH oxidase pathways, contributes to inflammatory and profibrotic signaling during disease progression. This study investigated whether human placenta-derived mesenchymal stem cells (MSCs) could modulate oxidative stress and fibrotic responses in an experimental CKD model. Methods: A subtotal nephrectomy model was used to establish CKD in rats. Following disease induction, placenta-derived MSCs were administered intravenously. Renal tissues were evaluated for markers associated with oxidative injury, including ROS, hydrogen peroxide (H2 O2 ), and NADPH oxidase-4 (NOX4). Fibrosis-related molecules, including fibronectin, collagen IV, and α-smooth muscle actin (α-SMA), were also assessed and compared among study groups. Results: MSC administration was associated with reductions in oxidative stress markers, including ROS, H2 O2, and NOX4 expression. A trend toward reduced expression of fibrosis-related markers was also observed following MSC treatment; however, reductions in protein expression did not reach statistical significance for all comparisons. Conclusion: Placenta-derived MSC treatment was associated with modulation of oxidative stress– and fibrosis-related pathways in experimental CKD. Although reductions in several molecular markers were observed following treatment, additional studies with larger sample sizes and longer follow-up periods are needed to confirm the therapeutic potential of MSCs and to further clarify their effects on renal fibrosis and disease progression.