Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5826518 | Current Opinion in Pharmacology | 2009 | 7 Pages |
Abstract
The kinin B1 receptor plays an important role in mediating the inflammatory effects of the kallikrein-kinin pathway. The recent development of orally available non-peptidic antagonists and genetically modified mice deficient in B1 receptor expression have demonstrated that the receptor plays a pivotal role in the cellular, particularly neutrophil, recruitment associated with an acute inflammatory response. These tools have also enabled elucidation of the pathways involved in mediating this effect and have highlighted a major role for chemokines, particularly CXCL5 and CCL2. Neutrophil recruitment is involved in the pathogenesis of renal disease and has very recently been implicated in the early stages of atherosclerosis. In this review we discuss the most recent evidence linking the B1 receptor with the pathogenesis of these two inflammatory cardiovascular diseases and highlight the therapeutic potential of the kinin B1 receptor in these disease states.
Related Topics
Life Sciences
Neuroscience
Cellular and Molecular Neuroscience
Authors
Johan Duchene, Amrita Ahluwalia,