Early Effects of Extracellular Vesicles Secreted by Adipose Tissue Mesenchymal Cells in Renal Ischemia Followed by Reperfusion: Mechanisms Rely in the Restoration of the Redox Tissular Environment

Bone Marrow Mononuclear Cells Restore Normal Mitochondrial Ca2+ Handling and Ca2+-Induced Depolarization of the Internal Mitochondrial Membrane by Inhibiting the Permeability Transition Pore After Ischemia/Reperfusion

“…The target for the alterations by IR of the renal mitochondrial Ca 2+ influx is possibly the mitochondrial Ca 2+ uniporter (MCU) 37,38 , its tetrameric structure preserved from fungi to humans 39,40 being destabilized by the intense production of ROS after IR. In a recent communication 41 , we demonstrated that intense oxidative stress is responsible for the early lesions caused by IR, which is avoided by administration of the main paracrine secretion of stem and mesenchymal cells (MSC)-the EVs they secrete 42 . BMMC, which contains a small parcel of MSC 43 , has the same effect in preserving renal structures 14,15,17,22,44 , demonstrating that they contain a population of cells that helps in the preservation of renal structure and function.…”

“…In conclusion, we have demonstrated that BMMC prevent renal mitochondrial lesions during the AKI caused by IR through mechanisms associated with the preservation of Ca 2+ influx and release, and with the response of ΔΨ to Ca 2+ . It is possible that the preservation of these mechanisms relies-at least in part-on the control of the microenvironmental production of ROS 41 in early periods after IR.…”