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. 2020 Feb 27;11:74. doi: 10.3389/fimmu.2020.00074

Table 4.

Studies on MSC-derived EVs as therapeutic tool in AKI from IRI.

MSC origin Mechanism References
Human bone marrow Reduced apoptosis and increased proliferation of renal tubule epithelial cells (166)
Rat bone marrow Reduced inflammatory cytokines (IL1β; TNFα) (182)
Human umbilical cord Antioxidation through activation of Nrf2/antioxidant response elements (ARE) and decreased expression of NOX2 (183, 184)
Human umbilical cord Decreased renal fibrosis (downregulation of CX3CL1, decrease of CD68+macrophages); increased angiogenesis (increased expression of renal VEGF) (185187)
Human umbilical cord Tubular cell dedifferentiation and growth (increased ERK1/2 and HGE expression) (188)
Human umbilical cord Inhibition of mitochondrial fission (miR-30) and reduced apoptosis (176)
Mouse kidney resident Increased proliferation and reduced apoptosis; increased angiogenesis (189)
Mouse kidney resident (glomeruli) Increased proliferation of renal tubule epithelial cells (190)
Rat adipose tissue Inhibition of oxidative stress, apoptosis, renal fibrosis (191)
Human umbilical cord Increased proliferation and fibrosis (releasing from G2/M cell cycle arrest) (192)
Human bone marrow Inhibition of apoptosis (downregulation of Sema3A expression and activation of AKT/ERK pathways through miR-199a-3p); inhibition of NK (193)
Human umbilical cord Inhibition of apoptosis, increased proliferation of renal tubule epithelial cells; reduced CD68+macrophages infiltration; reduced fibrosis (decreased expression of aSMA and TGFβ; increased expression of HGF) (194)
Human BM Suppression of endoplasmic reticulum stress (miR-199a-5p) (177)