Titre
Translational implications of endothelial cell dysfunction in association with chronic allograft rejection
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Bruneau, S.
Auteure/Auteur
Wedel, J.
Auteure/Auteur
Fakhouri, F.
Auteure/Auteur
Nakayama, H.
Auteure/Auteur
Boneschansker, L.
Auteure/Auteur
Irimia, D.
Auteure/Auteur
Daly, K. P.
Auteure/Auteur
Briscoe, D. M.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
1432-198X
Statut éditorial
Publié
Date de publication
2016-01
Volume
31
Numéro
1
Première page
41
Dernière page/numéro d’article
51
Langue
anglais
Notes
Bruneau, Sarah
Wedel, Johannes
Fakhouri, Fadi
Nakayama, Hironao
Boneschansker, Leo
Irimia, Daniel
Daly, Kevin P
Briscoe, David M
eng
R01AI92305/AI/NIAID NIH HHS/
R21 AI114223/AI/NIAID NIH HHS/
T32DK007726/DK/NIDDK NIH HHS/
R01AI046756/AI/NIAID NIH HHS/
T32 AI007529/AI/NIAID NIH HHS/
R21 AG051082/AG/NIA NIH HHS/
T32AI007529/AI/NIAID NIH HHS/
R01 GM092804/GM/NIGMS NIH HHS/
T32 DK007726/DK/NIDDK NIH HHS/
R01 AI046756/AI/NIAID NIH HHS/
R01 AI092305/AI/NIAID NIH HHS/
R21AI114223/AI/NIAID NIH HHS/
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Germany
Pediatr Nephrol. 2016 Jan;31(1):41-51. doi: 10.1007/s00467-015-3094-6. Epub 2015 Apr 24.
Wedel, Johannes
Fakhouri, Fadi
Nakayama, Hironao
Boneschansker, Leo
Irimia, Daniel
Daly, Kevin P
Briscoe, David M
eng
R01AI92305/AI/NIAID NIH HHS/
R21 AI114223/AI/NIAID NIH HHS/
T32DK007726/DK/NIDDK NIH HHS/
R01AI046756/AI/NIAID NIH HHS/
T32 AI007529/AI/NIAID NIH HHS/
R21 AG051082/AG/NIA NIH HHS/
T32AI007529/AI/NIAID NIH HHS/
R01 GM092804/GM/NIGMS NIH HHS/
T32 DK007726/DK/NIDDK NIH HHS/
R01 AI046756/AI/NIAID NIH HHS/
R01 AI092305/AI/NIAID NIH HHS/
R21AI114223/AI/NIAID NIH HHS/
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Germany
Pediatr Nephrol. 2016 Jan;31(1):41-51. doi: 10.1007/s00467-015-3094-6. Epub 2015 Apr 24.
Résumé
Advances in therapeutics have dramatically improved short-term graft survival, but the incidence of chronic rejection has not changed in the past 20 years. New insights into mechanism are sorely needed at this time and it is hoped that the development of predictive biomarkers will pave the way for the emergence of preventative therapeutics. In this review, we discuss a paradigm suggesting that sequential changes within graft endothelial cells (EC) lead to an intragraft microenvironment that favors the development of chronic rejection. Key initial events include EC injury, activation and uncontrolled leukocyte-induced angiogenesis. We propose that all of these early changes in the microvasculature lead to abnormal blood flow patterns, local tissue hypoxia, and an associated overexpression of HIF-1alpha-inducible genes, including vascular endothelial growth factor. We also discuss how cell intrinsic regulators of mTOR-mediated signaling within EC are of critical importance in microvascular stability and may thus have a role in the inhibition of chronic rejection. Finally, we discuss recent findings indicating that miRNAs may regulate EC stability, and we review their potential as novel non-invasive biomarkers of allograft rejection. Overall, this review provides insights into molecular events, genes, and signals that promote chronic rejection and their potential as biomarkers that serve to support the future development of interruption therapeutics.
Sujets
PID Serval
serval:BIB_33C6FA51CAB9
PMID
Date de création
2022-03-01T09:18:05.957Z
Date de création dans IRIS
2025-05-20T14:25:29Z