Mesenchymal Stem Cells: a Promising Therapeutic Tool for Acute Kidney Injury.
Selim RE., Ahmed HH., Abd-Allah SH., Sabry GM., Hassan RE., Khalil WKB.
Animal Study with a reported sample of 10 on Chronic Kidney Disease, Acute Kidney Injury, published in Appl Biochem Biotechnol (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Appl Biochem Biotechnol (2019)
- Country
- United States
- Reported sample size
- 10
- Source database
- PubMed
- PMID
- 30976980
- DOI
- 10.1007/s12010-019-02995-2
Abstract (original English)
Acute kidney injury (AKI) is a rapid loss of renal function. It has high mortality rates. Still, renal replacement therapy is considered the best solution for recovering AKI. This opens a line of thought to develop an alternative therapy for it without complications. Mesenchymal stem cells are considered a new therapy for treating kidney diseases. The aim of this work was to address the anti-apoptotic, antioxidative, and pro-angiogenic effects of adipose tissue-derived MSCs (AD-MSCs) and bone marrow-MSCs (BM-MSCs) for treating AKI. Adult male Wistar rats were assigned into nine groups (n = 10): (1) the control group; (2) the AKI group, receiving cisplatin; (3) the AKI group treated with AD-MSCs (1 × 10 6 ); (4) the AKI group treated with AD-MSCs (2 × 10 6 ); (5) the AKI group treated with AD-MSCs (4 × 10 6 ); (6) the AKI group treated with losartan; (7) the AKI group treated with BM-MSCs (1 × 10 6 ); (8) the AKI group treated with BM-MSCs (2 × 10 6 ); and (9) the AKI group treated with BM-MSCs (4 × 10 6 ). The results showed a significant rise in creatinine, urea, and cystatin C (cys C) levels and upregulation of p38 mRNA, whereas a significant decline in NAD(P)H quinone oxidoreductase 1 (NQO-1) protein and downregulation of B-cell lymphoma-2 (Bcl-2) mRNA and vascular endothelial growth factor (VEGF) mRNA were recorded in AKI. MSCs could improve renal functions manifested by de
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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