Ginkgolic Acids Impair Mitochondrial Function by Decreasing Mitochondrial Biogenesis and Promoting FUNDC1-Dependent Mitophagy
Ginkgolic Acids Impair Mitochondrial Function by Decreasing Mitochondrial Biogenesis and Promoting FUNDC1-Dependent Mitophagy
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银杏酸通过减少线粒体生物发生和促进 FUNDC1 依赖性线粒体自噬来损害线粒体功能
DOI：
10.1021/acs.jafc.9b04178
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发表时间：
2019
影响因子：
6.1
通讯作者：
Zhou Qinghua
中科院分区：
文献类型：
--
作者：
Wang Wenjun;Wang Miaomiao;Ruan Yu;Tan Junyang;Wang Hao;Yang Tao;Li Jianshuang;Zhou Qinghua
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Ginkgolic acids (GAs) are found in the leaves, nuts, and testa ofGinkgo bilobaand have been reported to exhibit antitumor, antibacterial, and pro-apoptotic activities. However, their role in mitochondrial function is still unclear. Our previous study showed that genes related to the mitochondria present significant changes in GA-treated mouse bone marrow stromal cells. We hypothesize that GAs may regulate mitochondrial function. Here, we found that GA treatment induced mitochondrial fragmentation, reduced mtDNA copy numbers and mitochondrial protein levels, and impaired mitochondrial adenosine 5′-triphosphate production and oxygen consumption. The GA-induced mitochondrial mass loss may be due to decreased mitochondrial biogenesis. In addition, abolishing autophagy by Atg7 knockout or the administration of an autophagy inhibitor can restore the GA-induced decrease in mitochondrial mass. Furthermore, FUNDC1 knockdown restored the GA-induced changes in mitochondrial mass reduction and mitochondrial membrane potential loss. Together, our studies demonstrated that GAs impaired mitochondrial function by decreasing mitochondrial biogenesis and promoting FUNDC1-dependent mitophagy.