Extracellular vesicles from hypoxia-preconditioned mesenchymal stem cells preserve mitochondrial functions and redox homeostasis in ischemia-reperfusion-induced acute kidney injury.
Andrade-Soares M., Alves M., Rodrigues-Ferreira C., Lopes JA., Crisóstomo T., Costa-Sarmento G.
Animal Study on Acute Kidney Injury, published in Biochim Biophys Acta Gen Subj (2026) — summary generated from the PubMed abstract.
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- Study type
- Animal Study
- Journal
- Biochim Biophys Acta Gen Subj (2026)
- Country
- Netherlands
- Reported sample size
- —
- PMID
- 41173062
- DOI
- 10.1016/j.bbagen.2025.130874
Abstract (original English)
Acute kidney injury (AKI) induced by ischemia-reperfusion (I/R) remains a significant clinical challenge due to its rapid progression, limited therapeutic options, and high morbidity. Mitochondrial dysfunction is a critical component of AKI pathogenesis, contributing to oxidative stress, impaired bioenergetics, and tissue injury. Extracellular vesicles (EV) derived from mesenchymal stem cells (MSC) have emerged as potential candidates for organ protection through the modulation of inflammatory and oxidative pathways. This study evaluated the effects of EV secreted by hypoxia-preconditioned adipose-derived MSC on mitochondrial function in a rat model of I/R-induced AKI. Wistar rats were assigned to four groups: SHAM, I/R, SHAM + EV, and I/R + EV. Hypoxia-preconditioned EV (2 × 10 9 ) or vehicle were administered subcapsularly 1 h prior to bilateral renal artery clamping (45 min ischemia, 1 h reperfusion). Histological analyses demonstrated that EV treatment effectively prevented tubular injury, inflammatory infiltration, and preserved renal architecture. EV enhanced Nrf2 nuclear translocation, upregulated HO-1 expression, and stabilized antioxidant defenses. Furthermore, EV preserved mitochondrial membrane potential, respiratory control ratio, ATP synthesis, and the abundance of electron transport chain complexes I, III, and IV, although complex II remained vulnerable. Proton le
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 comes from animal or laboratory studies and has not been confirmed in humans.
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