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: D N Müller, R Dechend, A Fiebeler, J K Park, H Haller, F C Luft
• Journal: Advances in nephrology from the Necker Hospital (Adv Nephrol Necker Hosp) Vol. 31 Pg. 89-103 ( 2001) ISSN: 0084-5957 [Print] United States
• PMID: 11692473 (Publication Type: Journal Article, Review)

Chemical References

• MAS1 protein, human
• Proto-Oncogene Mas
• Angiotensin II

Topics

• Angiotensin II (immunology)
• Animals
• Humans
• Hypertension, Renal (immunology, therapy)
• Proto-Oncogene Mas