Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia-reperfusion injury in rats via the mTOR pathway.

Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia-reperfusion injury in rats via the mTOR pathway. J Cell Mol Med. 2019 Mar 19;: Authors: Liu WC, Chen SB, Liu S, Ling X, Xu QR, Yu BT, Tang J Abstract Impaired mitochondrial function is a key factor attributing to lung ischaemia-reperfusion (IR) injury, which contributes to major post-transplant complications. Thus, the current study was performed to investigate the role of mitochondrial autophagy in lung I/R injury and the involvement of the mTOR pathway. We established rat models of orthotopic left lung transplantation to investigate the role of mitochondrial autophagy in I/R injury following lung transplantation. Next, we treated the donor lungs with 3-MA and Rapamycin to evaluate mitochondrial autophagy, lung function and cell apoptosis with different time intervals of cold ischaemia preservation and reperfusion. In addition, mitochondrial autophagy, and cell proliferation and apoptosis of pulmonary microvascular endothelial cells (PMVECs) exposed to hypoxia-reoxygenation (H/R) were monitored after 3-MA administration or Rapamycin treatment. The cell apoptosis could be inhibited by mitochondrial autophagy at the beginning of lung ischaemia, but was rendered out of control when mitochondrial autophagy reached normal levels. After I/R of donor lung, the mitochondrial autophagy was increased until 6 hours after reperfusion and then ...
Source: J Cell Mol Med - Category: Molecular Biology Authors: Tags: J Cell Mol Med Source Type: research