Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation

The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia–reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft func...

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Main Authors: Dario Troise, Costanza Allegra, Luciana Antonia Cirolla, Silvia Mercuri, Barbara Infante, Giuseppe Castellano, Giovanni Stallone
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Antioxidants
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Online Access:https://www.mdpi.com/2076-3921/14/1/66
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author Dario Troise
Costanza Allegra
Luciana Antonia Cirolla
Silvia Mercuri
Barbara Infante
Giuseppe Castellano
Giovanni Stallone
author_facet Dario Troise
Costanza Allegra
Luciana Antonia Cirolla
Silvia Mercuri
Barbara Infante
Giuseppe Castellano
Giovanni Stallone
author_sort Dario Troise
collection DOAJ
description The complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia–reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, particularly the alternative pathway, participates in the pathogenesis of IRI, involving all kidney compartments. In particular, tubular epithelial cells often acquire a dysfunctional phenotype that can exacerbate complement activation and kidney damage. Currently, complement-modulating drugs are under investigation for the treatment of kidney diseases. Many of these drugs have shown potential therapeutic benefits, but no effective clinical treatments for renal IRI have been identified yet. In this review, we will explore drugs that target complement factors, complement receptors, and regulatory proteins, aiming to highlight their potential value in improving the management of renal IRI.
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series Antioxidants
spelling doaj-art-8112de697d2c4557b8d02b52d641624a2025-01-24T13:19:22ZengMDPI AGAntioxidants2076-39212025-01-011416610.3390/antiox14010066Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney TransplantationDario Troise0Costanza Allegra1Luciana Antonia Cirolla2Silvia Mercuri3Barbara Infante4Giuseppe Castellano5Giovanni Stallone6Nephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyUnit of Nephrology, Dialysis and Transplantation, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico di Milano, 20122 Milan, ItalyNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, ItalyThe complement system plays a crucial role in regulating the inflammatory responses in kidney transplantation, potentially contributing to early decline in kidney function. Ischemia–reperfusion injury (IRI) is among the factors affecting graft outcomes and a primary contributor to delayed graft function. Complement activation, particularly the alternative pathway, participates in the pathogenesis of IRI, involving all kidney compartments. In particular, tubular epithelial cells often acquire a dysfunctional phenotype that can exacerbate complement activation and kidney damage. Currently, complement-modulating drugs are under investigation for the treatment of kidney diseases. Many of these drugs have shown potential therapeutic benefits, but no effective clinical treatments for renal IRI have been identified yet. In this review, we will explore drugs that target complement factors, complement receptors, and regulatory proteins, aiming to highlight their potential value in improving the management of renal IRI.https://www.mdpi.com/2076-3921/14/1/66kidney transplantationcomplement systemischemia–reperfusion injuryEculizumabiptacopancomplement-targeting drugs
spellingShingle Dario Troise
Costanza Allegra
Luciana Antonia Cirolla
Silvia Mercuri
Barbara Infante
Giuseppe Castellano
Giovanni Stallone
Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
Antioxidants
kidney transplantation
complement system
ischemia–reperfusion injury
Eculizumab
iptacopan
complement-targeting drugs
title Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
title_full Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
title_fullStr Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
title_full_unstemmed Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
title_short Exploring Potential Complement Modulation Strategies for Ischemia–Reperfusion Injury in Kidney Transplantation
title_sort exploring potential complement modulation strategies for ischemia reperfusion injury in kidney transplantation
topic kidney transplantation
complement system
ischemia–reperfusion injury
Eculizumab
iptacopan
complement-targeting drugs
url https://www.mdpi.com/2076-3921/14/1/66
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