Endothelial Dysfunction in Kidney Transplantation
Kidney transplantation entails a high likelihood of endothelial injury. The endothelium is a target of choice for injury by ischemia-reperfusion, alloantibodies, and autoantibodies. A certain degree of ischemia-reperfusion injury inevitably occurs in the immediate posttransplant setting and can mani...
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doaj-31dc0b2bb00d46498ae1b068835fd3832020-11-24T23:31:57ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-05-01910.3389/fimmu.2018.01130342152Endothelial Dysfunction in Kidney TransplantationHéloïse Cardinal0Héloïse Cardinal1Héloïse Cardinal2Mélanie Dieudé3Mélanie Dieudé4Marie-Josée Hébert5Marie-Josée Hébert6Marie-Josée Hébert7Research Centre, Centre hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, CanadaCanadian National Transplant Research Program, Montreal, QC, CanadaUniversity of Montreal, Montreal, QC, CanadaResearch Centre, Centre hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, CanadaCanadian National Transplant Research Program, Montreal, QC, CanadaResearch Centre, Centre hospitalier de l’Université de Montréal (CRCHUM), Montreal, QC, CanadaCanadian National Transplant Research Program, Montreal, QC, CanadaUniversity of Montreal, Montreal, QC, CanadaKidney transplantation entails a high likelihood of endothelial injury. The endothelium is a target of choice for injury by ischemia-reperfusion, alloantibodies, and autoantibodies. A certain degree of ischemia-reperfusion injury inevitably occurs in the immediate posttransplant setting and can manifest as delayed graft function. Acute rejection episodes, whether T-cell or antibody-mediated, can involve the graft micro- and macrovasculature, leading to endothelial injury and adverse long-term consequences on graft function and survival. In turn, caspase-3 activation in injured and dying endothelial cells favors the release of extracellular vesicles (apoptotic bodies and apoptotic exosome-like vesicles) that further enhance autoantibody production, complement deposition, and microvascular rarefaction. In this review, we present the evidence for endothelial injury, its causes and long-term consequences on graft outcomes in the field of kidney transplantation.https://www.frontiersin.org/article/10.3389/fimmu.2018.01130/fullkidney transplantationendothelial injuryapoptosisnecroptosisalloantibodiesautoantibodies |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Héloïse Cardinal Héloïse Cardinal Héloïse Cardinal Mélanie Dieudé Mélanie Dieudé Marie-Josée Hébert Marie-Josée Hébert Marie-Josée Hébert |
spellingShingle |
Héloïse Cardinal Héloïse Cardinal Héloïse Cardinal Mélanie Dieudé Mélanie Dieudé Marie-Josée Hébert Marie-Josée Hébert Marie-Josée Hébert Endothelial Dysfunction in Kidney Transplantation Frontiers in Immunology kidney transplantation endothelial injury apoptosis necroptosis alloantibodies autoantibodies |
author_facet |
Héloïse Cardinal Héloïse Cardinal Héloïse Cardinal Mélanie Dieudé Mélanie Dieudé Marie-Josée Hébert Marie-Josée Hébert Marie-Josée Hébert |
author_sort |
Héloïse Cardinal |
title |
Endothelial Dysfunction in Kidney Transplantation |
title_short |
Endothelial Dysfunction in Kidney Transplantation |
title_full |
Endothelial Dysfunction in Kidney Transplantation |
title_fullStr |
Endothelial Dysfunction in Kidney Transplantation |
title_full_unstemmed |
Endothelial Dysfunction in Kidney Transplantation |
title_sort |
endothelial dysfunction in kidney transplantation |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Immunology |
issn |
1664-3224 |
publishDate |
2018-05-01 |
description |
Kidney transplantation entails a high likelihood of endothelial injury. The endothelium is a target of choice for injury by ischemia-reperfusion, alloantibodies, and autoantibodies. A certain degree of ischemia-reperfusion injury inevitably occurs in the immediate posttransplant setting and can manifest as delayed graft function. Acute rejection episodes, whether T-cell or antibody-mediated, can involve the graft micro- and macrovasculature, leading to endothelial injury and adverse long-term consequences on graft function and survival. In turn, caspase-3 activation in injured and dying endothelial cells favors the release of extracellular vesicles (apoptotic bodies and apoptotic exosome-like vesicles) that further enhance autoantibody production, complement deposition, and microvascular rarefaction. In this review, we present the evidence for endothelial injury, its causes and long-term consequences on graft outcomes in the field of kidney transplantation. |
topic |
kidney transplantation endothelial injury apoptosis necroptosis alloantibodies autoantibodies |
url |
https://www.frontiersin.org/article/10.3389/fimmu.2018.01130/full |
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