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.

使用MA-5处理通过上调自噬作用减少了线粒体凋亡。提高的自噬作用降解了受损的线粒体，打断了线粒体凋亡，中和了ROS过度产生，并提高了细胞的能量产生。我们还发现MA-5通过MAPK-ERK-Yap信号通路调控自噬作用是受到Bnip3的控制。抑制该信号通路或降低Bnip3表达阻止了MA-5对线粒体稳态的有益效果，并增加了微胶质细胞凋亡[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].