摘要
Hypoxia leads to decreased synthesis of 5-Methoxytryptophan (5-MTP) in pulmonary microvascular endothelial cells by downregulating Asmt level via Hif1α induced NF-κB p50 nuclear translocation. 5-MTP can reduce the localization of Prdx6 to lysosomes and increase its protein level by reducing its lysosomal degradation through interacting with Prdx6-S32, without affecting its function of clearing lipid peroxides (LPOs), thus improving the lipid peroxidation and rescuing VE-cadherin level and endothelial barrier function.
危险品化学品经营许可证(带存储)