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. 2017 May 4;313(2):L252–L266. doi: 10.1152/ajplung.00453.2016

Fig. 7.

Fig. 7.

Proposed model. METH enters PMVECs and is metabolized to p-OHMA and other toxic metabolites, which trigger reactive oxygen species (ROS) production and an autophagy response. CES1 (green) is required to reduce ROS production and maintain steady autophagy flux. Reduced CES1 expression and/or activity (red) result in increased ROS production and abnormal autophagy flux, resulting in increased PMVEC apoptosis and loss of pulmonary microvessels.