title: [Involvement of endoplasmic reticulum stress in solid organ transplantation].
abstract: Endoplasmic reticulum (ER) stress is a situation caused by the accumulation of unfolded proteins in the endoplasmic reticulum, triggering an evolutionary conserved adaptive response termed the unfolded protein response. When adaptation fails, excessive and prolonged ER stress triggers cell suicide. Important roles for ER-initiated cell death pathways have been recognized for several diseases, including diabetes, hypoxia, ischemia/reperfusion injury, neurodegenerative and heart diseases. The implication of the ER stress is not well recognized in solid organ transplantation, but increasing evidence suggests its implication in mediating allograft injury. The purpose of this review is to summarize the mechanisms of ER stress and to discuss its implication during tissue injury in solid organ transplantation. The possible implications of the ER stress in the modifications of cell functional properties and phenotypic changes are also discussed beyond the scope of adaptation and cell death. Increasing the understanding of the cellular and molecular mechanisms of acute and chronic allograft damages could lead to the development of new biomarkers and to the discovery of new therapeutic strategies to prevent the initiation of graft dysfunction or to promote the tissue regeneration after injury.
authors.affiliation: Inserm U775, Centre universitaire des Saints-Pères, Paris, France. nicolas.pallet@univ-paris5.fr
authors.forename: Nicolas
authors.initials: N
authors.lastname: Pallet
authors.forename: Nicolas
authors.initials: N
authors.lastname: Bouvier
authors.forename: Philippe
authors.initials: P
authors.lastname: Beaune
authors.forename: Christophe
authors.initials: C
authors.lastname: Legendre
authors.forename: Dany
authors.initials: D
authors.lastname: Anglicheau
authors.forename: Eric
authors.initials: E
authors.lastname: Thervet
mesh_terms: D000818:Animals; D017209:Apoptosis; D016572:Cyclosporine / Q000009:adverse effects; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000209:etiology; D016503:Drug Delivery Systems; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000502:physiology*; D006085:Graft Survival; D006801:Humans; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000187:drug effects; D016030:Kidney Transplantation; D016031:Liver Transplantation; D051379:Mice; D009926:Organ Preservation; D011183:Postoperative Complications / Q000473:pathology / Q000517:prevention & control; D015427:Reperfusion Injury / Q000473:pathology; D016559:Tacrolimus / Q000009:adverse effects; D014180:Transplantation; D014184:Transplantation, Homologous / Q000473:pathology; D056811:Unfolded Protein Response / Q000187:drug effects / Q000502:physiology*
chemical_list: D016572:Cyclosporine; D016559:Tacrolimus