title: Nitric oxide and the resolution of inflammation: implications for atherosclerosis.
abstract: The ubiquitous free radical, nitric oxide (NO), plays an important role in many biological processes including the regulation of the inflammatory response. Alterations in NO synthesis by endogenous systems likely influence inflammatory processes occurring in a wide range of diseases including many in the cardiovascular system (e.g. atherosclerosis). Progression of inflammatory conditions depends not only upon the recruitment and activation of inflammatory cells but also upon their subsequent removal from the inflammatory milieu. Apoptosis, or programmed cell death, is a fundamental process regulating inflammatory cell survival and is critically involved in ensuring the successful resolution of an inflammatory response. Apoptosis results in shutdown of secretory pathways and renders effete, but potentially highly histotoxic, cells instantly recognisable for non-inflammatory clearance by phagocytes (e.g., macrophages). However, dysregulation of apoptosis and phagocytic clearance mechanisms can have drastic consequences for development and resolution of inflammatory processes. In this review we highlight the complexities of NO-mediated regulation of inflammatory cell apoptosis and clearance by phagocytes and discuss the molecular mechanisms controlling these NO mediated effects. We believe that manipulation of pathways involving NO may have previously unrecognised therapeutic potential for limiting or resolving inflammatory and cardiovascular disease.
authors.affiliation: Centre for Cardiovascular Science, University of Edinburgh, Teviot Place, Scotland, UK.
authors.forename: Catherine A
authors.initials: CA
authors.lastname: Shaw
authors.forename: Emma L
authors.initials: EL
authors.lastname: Taylor
authors.forename: Ian L
authors.initials: IL
authors.lastname: Megson
authors.forename: Adriano G
authors.initials: AG
authors.lastname: Rossi
mesh_terms: D017209:Apoptosis / Q000502:physiology*; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*
chemical_list: D009569:Nitric Oxide