title: Inflammation and angiotensin II.
abstract: Angiotensin II (AngII), the major effector peptide of renin-angiotensin system (RAS), is now recognized as a growth factor that regulates cell growth and fibrosis, besides being a physiological mediator restoring circulatory integrity. In the last few years, a large number of experimental studies has further demonstrated that AngII is involved in key events of the inflammatory process. Here, we summarize the wide variety of AngII functions and discuss them in relation with the inflammatory cascade. AngII increases vascular permeability (via the release of prostaglandins and vascular endothelial cell growth factor or rearrangement of cytoskeletal proteins) that initiates the inflammatory process. AngII could contribute to the recruitment of inflammatory cells into the tissue through the regulation of adhesion molecules and chemokines by resident cells. Moreover, AngII could directly activate infiltrating immunocompetent cells, including chemotaxis, differentiation and proliferation. Recent data also suggest that RAS activation could play a certain role even in immunologically-induced inflammation. Transcriptional regulation, predominantly via nuclear factor-kappaB (NF-kappaB) and AP-1 activation, and second mediator systems, such as endothelin-1, the small G protein (Rho) and redox-pathways are shown to be involved in the molecular mechanism by which AngII exerts those functions. Finally, AngII participates in tissue repair and remodeling, through the regulation of cell growth and matrix synthesis. In summary, recent data support the hypothesis that RAS is key mediator of inflammation. Further understanding of the role of the RAS in this process may provide important opportunities for clinical research and treatment of inflammatory diseases.
authors.affiliation: Renal and Vascular Research Laboratory, Fundación Jiménez Díaz, Autonoma University, Avda Reyes Católicos 2, 28040 Madrid, Spain.
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Marta
authors.initials: M
authors.lastname: Ruiz-Ortega
authors.forename: Oscar
authors.initials: O
authors.lastname: Lorenzo
authors.forename: Monica
authors.initials: M
authors.lastname: Ruperez
authors.forename: Vanesa
authors.initials: V
authors.lastname: Esteban
authors.forename: Jesus
authors.initials: J
authors.lastname: Egido
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D002199:Capillary Permeability; D002448:Cell Adhesion / Q000276:immunology; D018925:Chemokines / Q000096:biosynthesis / Q000276:immunology; D016228:Endothelial Growth Factors / Q000096:biosynthesis / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000502:physiology; D008222:Lymphokines / Q000096:biosynthesis / Q000502:physiology; D020556:Neutrophil Infiltration / Q000276:immunology; D007703:Peptidyl-Dipeptidase A; D011453:Prostaglandins / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D018925:Chemokines; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D011453:Prostaglandins; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A