Endoplasmic reticulum stress: an unrecognized actor in solid organ transplantation.
Endoplasmic reticulum (ER) stress is an adaptive response to the accumulation of misfolded proteins within the ER, which can trigger cell dedifferentiation and cell suicide. Increasing evidences suggest its implication in mediating allograft injury. Herein, we summarize the mechanisms of ER stress and discuss its implication in allograft injury. Increasing our 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.
Pallet
Nicolas
N
INSERM U775 and Université Paris Descartes, Centre Universitaire des Saints-Pères, Paris, France. nicolas.pallet@univ-paris5.fr
Fougeray
Sophie
S
Beaune
Philippe
P
Legendre
Christophe
C
Thervet
Eric
E
Anglicheau
Dany
D
D000818:Animals; D065095:Calcineurin Inhibitors; D002908:Chronic Disease; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D007668:Kidney / Q000473:pathology; D008954:Models, Biological; D011489:Protein Denaturation; D017510:Protein Folding; D012038:Regeneration; D015427:Reperfusion Injury; D013312:Stress, Physiological; D014180:Transplantation / Q000379:methods*; D014184:Transplantation, Homologous / Q000379:methods
D065095:Calcineurin Inhibitors