Inflammaging and Complement System: A Link Between Acute Kidney Injury and Chronic Graft Damage.
Acute Kidney Injury
/ complications
Aging
/ immunology
Animals
Complement Activation
Complement Inactivating Agents
/ therapeutic use
Complement System Proteins
/ metabolism
Delayed Graft Function
/ drug therapy
Disease Progression
Epigenesis, Genetic
/ immunology
Humans
Kidney
/ immunology
Kidney Transplantation
Mice
Renal Insufficiency, Chronic
/ drug therapy
Reperfusion Injury
/ immunology
AKI-to-CKD transition
cellular senescence and SASP
complement inhibition therapy
complement system
renal aging
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
02
11
2019
accepted:
31
03
2020
entrez:
28
5
2020
pubmed:
28
5
2020
medline:
1
4
2021
Statut:
epublish
Résumé
The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney's excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16
Identifiants
pubmed: 32457738
doi: 10.3389/fimmu.2020.00734
pmc: PMC7221190
doi:
Substances chimiques
Complement Inactivating Agents
0
Complement System Proteins
9007-36-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
734Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2020 Franzin, Stasi, Fiorentino, Stallone, Cantaluppi, Gesualdo and Castellano.
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