Angiotensin-induced inflammation and novel approaches to treatment.
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.
Müller
D N
DN
Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité, Humboldt University of Berlin.
Dechend
R
R
Fiebeler
A
A
Park
J K
JK
Haller
H
H
Luft
F C
FC
D000804:Angiotensin II / Q000276:immunology*; D000818:Animals; D006801:Humans; D006977:Hypertension, Renal / Q000276:immunology* / Q000628:therapy*; D000090063:Proto-Oncogene Mas
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D000804:Angiotensin II