HMOX1 and acute kidney injury: Part of the protective mechanism was due to the antioxidant, anti‐apoptosis and anti‐inflammatory effects of HO‐1 overexpression.51 Recently, these authors published a new paper, which documented that modification with HO‐1 significantly attenuated cell‐cycle arrest, activated PI3K/Akt and MEK/ERK pathways and enhanced the survival of MSCs, all of which helped to improve the therapeutic effect of BMSCs on I/R‐induced AKI.52