Mitochonic acid 5 (MA-5) is a derivative of the plant hormone indole-3-acetic acid. Mitochonic acid 5 binds mitochondria and ameliorates renal tubular and cardiac myocyte damage.It has been shown to improve survival of fibroblasts from patients with mitochondrial diseases.

Treatment with MA-5 reduced mitochondrial apoptosis via upregulation of mitophagy.?Increased mitophagy degraded damaged mitochondria, disrupting mitochondrial apoptosis, neutralizing ROS overproduction, and improving cellular energy production.?We also identified that MA-5 regulated mitophagy via Bnip3 through the MAPK-ERK-Yap signaling pathway.?Inhibiting this signaling pathway or knocking down Bnip3 expression prevented MA-5 from having beneficial effects on mitochondrial homeostasis and increased microglial apoptosis[1].

TNFα was used to induce inflammatory injury in mouse microglial BV-2 cells with and without prior MA-5 treatment. Cellular apoptosis was assessed using the MTT and TUNEL assays. Mitochondrial functions were evaluated via mitochondrial membrane potential JC-1 staining, ROS flow cytometry analysis, mPTP opening assessment, and immunofluorescence of cyt-c. Mitophagy was examined using western blots and immunofluorescence. The pathways analysis was carried out using western blots and immunofluorescence with a pathway blocker[1].