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Pimecrolimus Impaired Mitochondrion and Induced Mitophagy via AMPK Signaling Pathway
Wu Yanyang1, Hu Yongquan1, Zhou Haiyan1, Zhang Bo2*, Li Shao3*
1Food Science and Technology in Hunan Agriculture University, Changsha 410128, China; 2Tianjin International Joint Academy of Biotechnology and Medicine of High-throughput Molecular Drug Discovery Center, Tianjin 300457, China; 3Tsinghua National Laboratory for Information Technology, Beijing 100084, China
Abstract: Autophagy is a ubiquitous phenomenon in eukaryotes， which maintains the homeostasis of cells by degrading the misfolded and aging proteins or damaged organelles. It has been reported that calcineurin regulates autophagy， but its molecular mechanism has not been elucidated. It was reported that calcineurin inhibitors pimecrolimus induced autophagy via AMPK [adenosine 5′-monophosphate (AMP)-activated protein kinase] signaling pathway. Further study showed that pimecrolimus impaired mitochondrion and downregulated mitochondrial membrane gene Tim23 (mitochondrial inner membrane translocase complex， subunit 23) and this effect was inhibited by the autophagy inhibitor 3-MA (3-methyladenine) or stable knock down of AMPK expression. These results indicate that calcineurin inhibitor pimecrolimus regulates mitophagy via AMPK signaling pathway. The molecular mechanism of how calcineurin regulates mitophagy has been elucidated.
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