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

Antioxidants (Basel)

Nephrology, 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, Italy.

Published: January 2025

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.

Download full-text PDF

Source
http://dx.doi.org/10.3390/antiox14010066DOI Listing

Publication Analysis

Top Keywords

ischemia-reperfusion injury
8
kidney transplantation
8
complement activation
8
renal iri
8
complement
6
kidney
6
exploring potential
4
potential complement
4
complement modulation
4
modulation strategies
4

Similar Publications

Dihydromyricetin (Dih), a naturally occurring flavonoid, has been identified to exert a protective effect against ischemia/reperfusion injury. However, the detailed mechanisms remain unclear. Here we investigated the biological role of Dih in preventing hypoxia/reoxygenation (H/R) injury in cardiomyocytes.

View Article and Find Full Text PDF

Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.

View Article and Find Full Text PDF

Analysis of the protective effect of hydrogen sulfide over time in ischemic rat skin flaps.

Ann Chir Plast Esthet

January 2025

Department of Plastic, Reconstructive, and Aesthetic Surgery, Faculty of Medicine, Çukurova University, Adana, Turkey.

Background: Hydrogen sulfide (HS) is a widely studied gasotransmitter, and its protective effect against ischemia-reperfusion damage has been explored in several studies. Therefore, a requirement exists for a comprehensive study about HS effects on ischemia-reperfusion damage in flap surgery. The aim of this study is to examine the effect of hydrogen sulfide by creating ischemia-reperfusion injury in the vascular-stemmed island flap prepared from the rat groin area.

View Article and Find Full Text PDF

Sivelestat sodium protects against renal ischemia/reperfusion injury by reduction of NETs formation.

Arch Biochem Biophys

January 2025

Department of Critical Care Medicine, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150001, China; Heilongjiang Provincial Key Laboratory of Critical Care Medicine, Harbin 150001, China; Central Laboratory of The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China. Electronic address:

Background: Ischemia-reperfusion injury (IRI) often results in renal impairment. While the presence of neutrophil extracellular traps (NETs) is consistently observed, their specific impact on IRI is not yet defined. Sivelestat sodium, an inhibitor of neutrophil elastase which is crucial for NET formation, may offer a therapeutic approach to renal IRI, warranting further research.

View Article and Find Full Text PDF

Background: Myocardial ischemia-reperfusion (I/R) injury refers to cell damage that occurs as a consequence of the restoration of blood circulation following reperfusion therapy for cardiovascular diseases, and it is a primary cause of myocardial infarction. The search for nove therapeutic targets in the context of I/R injury is currently a highly active area of research. p70 ribosomal S6 kinase (S6K1) plays an important role in I/R induced necrosis, although the specific mechanisms remain unclear.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!