title: Angiogenic response following renal ischemia reperfusion injury: new players.
abstract: Ischemia-reperfusion (IR) injury can negatively influence the short- and long-term outcomes of kidney transplantation because it promotes acute tubular necrosis and tissue scarring and activates innate alloimmunity. The adaptive responses to IR are centrally involved in reducing tissue damage but can also be deleterious when they activate programmed cell death and inflammation. The HIF-1α-mediated angiogenic responses following IR at early and late stages are complex and poorly understood. The early stages of IR seem to be associated with an antiangiogenic response, whereas the hypoxia that follows IR at later stages may activate angiogenic factors such as vascular endothelial growth factor (VEGF) and may be beneficial by stabilizing the microvasculature and favoring local blood supply. In addition to HIF-1α, new players in angiogenesis, including mTOR and the unfolded protein response, may lead to innovative therapeutic strategies for treating patients with ischemia- and reperfusion-associated tissue inflammation and organ dysfunction.
authors.affiliation: Service de Biochimie, hôpital européen Georges Pompidou, Paris, France; Université Paris-Descartes, Sorbonne Paris Cité, Paris, France; INSERM U775, Centre universitaire des Saints-Pères, Paris, France. Electronic address: nicolas.pallet@parisdescartes.fr.
authors.forename: N
authors.initials: N
authors.lastname: Pallet
authors.affiliation: Université Paris-Descartes, Sorbonne Paris Cité, Paris, France; Service de Néphrologie, hôpital européen Georges Pompidou, université Paris-Descartes, Paris, France.
authors.forename: E
authors.initials: E
authors.lastname: Thervet
authors.affiliation: Université Paris-Descartes, Sorbonne Paris Cité, Paris, France; Service d'Urologie, hôpital européen Georges-Pompidou, université Paris-Descartes, Paris, France.
authors.forename: M-O
authors.initials: MO
authors.lastname: Timsit
mesh_terms: D004730:Endothelium, Vascular; D006801:Humans; D007668:Kidney / Q000098:blood supply*; D016030:Kidney Transplantation; D009389:Neovascularization, Pathologic / Q000209:etiology*; D015427:Reperfusion Injury / Q000150:complications*
keywords: Agents angiogéniques; Angiogenesis inducing agents; Ischemia-reperfusion injury; Kidney transplantation; Réponse aux protéines mal repliées; Transplantation rénale; Unfolded protein response; lésions d’ischémie-reperfusion