title: Endoplasmic reticulum stress enters a Nogo zone.
abstract: The debilitating disease pulmonary arterial hypertension (PAH) is characterized by an elevation in blood pressure in the lung arteries caused by vessel-blocking vascular-cell proliferation. This vascular remodeling is thought to result in part from defects in the endoplasmic reticulum stress response and mitochondrial dysfunction in pulmonary artery smooth muscle cells. In this issue of Science Translational Medicine, Sutendra et al. show that the vascular remodeling protein Nogo-B plays a role in the development of PAH in response to hypoxia-induced stress. The new findings finger Nogo-B as a possible therapeutic target for PAH.
authors.affiliation: Institute for Research in Biomedicine (IRB Barcelona) C/Baldiri Reixac 10, 08028 Barcelona, Spain.
authors.forename: Juan Pablo
authors.initials: JP
authors.lastname: Muñoz
authors.forename: Antonio
authors.initials: A
authors.lastname: Zorzano
mesh_terms: D000818:Animals; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D008928:Mitochondria / Q000378:metabolism*; D009185:Myelin Proteins / Q000378:metabolism*; D000070798:Nogo Proteins
chemical_list: D009185:Myelin Proteins; D000070798:Nogo Proteins; C000603199:RTN4 protein, human