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. 2021 Mar 11;11(11):5248–5266. doi: 10.7150/thno.54550

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Schematic illustration of the mechanism of MSC-exos for the treatment of ischemic AKI. In ischemic AKI, the injuries of TECs could lead to cell cycle arrest in G2/M phase and apoptosis. MSC-exos targeted injured kidney especially the proximal tubules due to VLA-4 and LFA-1 mediated adhesive interactions. Moreover, miR-125b-5p was enriched in MSC-exos and exerted tubular repair effect via suppressing the expression of p53, which not only up-regulated CDK1 and Cyclin B1 to rescue tubular G2/M arrest, but modulated Bcl-2 and Bax to inhibit TECs apoptosis.