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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Main Authors: Héloïse Cardinal, Mélanie Dieudé, Marie-Josée Hébert
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-05-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fimmu.2018.01130/full
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spelling 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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