title: Angiotensin-induced inflammation and novel approaches to treatment.
abstract: In a brief period, we have accrued a new view of Ang II. From conventional signaling pathways, our attention was directed toward signal transduction involving specific tyrosine kinases, inducing not only vasocontriction but also proto-oncogene expression, protein synthesis, hypertrophy and growth. More recently, our attention has been directed beyond these effects to inflammatory reactions involving NF-kappa B activation and related gene expression. The mechanisms are not known for certain but probably initially involve the generation of ROS. The subsequent NF-kappa B activation probably involves participation of endothelin signaling and, perhaps, NF-AT3 activation. It is possible that other compounds can also modulate Ang II-induced inflammatory responses.
authors.affiliation: Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité, Humboldt University of Berlin.
authors.forename: D N
authors.initials: DN
authors.lastname: Müller
authors.forename: R
authors.initials: R
authors.lastname: Dechend
authors.forename: A
authors.initials: A
authors.lastname: Fiebeler
authors.forename: J K
authors.initials: JK
authors.lastname: Park
authors.forename: H
authors.initials: H
authors.lastname: Haller
authors.forename: F C
authors.initials: FC
authors.lastname: Luft
mesh_terms: D000804:Angiotensin II / Q000276:immunology*; D000818:Animals; D006801:Humans; D006977:Hypertension, Renal / Q000276:immunology* / Q000628:therapy*; D000090063:Proto-Oncogene Mas
chemical_list: C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D000804:Angiotensin II