Similarly, the transfer of miR-30 from WJMSC-EVs has also been identified by Gu et al. Elevated levels of exogenous miR-30 in renal tubular cells could relieve the activation of dynamin-related protein-1 (DRP-1) and mitochondrial fragmentation induced by I/R-induced AKI, which led to antiapoptotic and renoprotective effects [62]. This evidence concerns the gene DNM1L and acute kidney injury.