MicroRNAs (miRNAs) are essential for the maintenance of podocyte homeostasis. Emerging evidence demonstrated a protective role of miRNA-30a, a member of miR-30 family in podocyte injury. However, the role of other members of miR-30 family in podocyte injury is unclear. The present study was undertaken to investigate the contribution of miR-30e in the pathogenesis of podocyte injury induced by aldosterone (Aldo), as well as the underlying mechanism. Following Aldo treatment, miR-30e was dose-and time-dependently reduced. Notably, overexpression of miR-30e remarkably attenuated Aldo-induced apoptosis in podocytes. In agreement with this finding, miR-30e silencing led to significant podocyte apoptosis. Mitochondrial dysfunction (MtD) has been shown as an early event in Aldo-induced podocyte injury. Here we found that overexpressing miR-30e improved Aldo-induced MtD while miR-30e silencing resulted in MtD. Next, we found that miR-30e could directly target BCL2/adenovirus E1B interacting protein 3-like (BNIP3L) gene. Aldo remarkably enhanced BNIP3L expression in podocytes and silencing BNIP3L largely abolished Aldo-induced MtD and cell apoptosis. On the contrary, overexpression of BNIP3L induced MtD and apoptosis in podocytes. Taken together, these findings demonstrated that miR-30e protected mitochondria and podocytes against Aldo challenge by targeting BNIP3L.