Renal Ischemia-Reperfusion Injury (IRI) is one of the main causes of Acute Kidney Injury
(AKI), and may lead to chronic kidney disease. The high mortality rate of AKI has not changed in the
last 5 decades due to non-recognition, nephrotoxin exposure, delayed diagnosis and lack of specific
intervention. Complement activation plays important roles in IRI-induced AKI because of its association
with immunity, inflammation, cell death and tissue repair. Nevertheless, the role of complement
properdin, the sole positive regulator of the alternative pathway, in IRI-induced AKI has not been well
defined. This review evaluates the dynamic changes and underlying mechanisms of complement activation
with a focus on properdin in both in vitro and in vivo models challenged by hypoxia/
reoxygenation and renal IRI. The multiple actions of properdin associated with HMGB1 and
caspase-3, apoptosis and inflammation mediators, are discussed in the context of immunity, injury and
repair at both the early and later stages of AKI. The complement activation-independent role of properdin
and the effect of modulating properdin with or without genotype alteration are also addressed.
Taking together, these might provide new mechanistic insights that potentially benefit timely diagnosis
and specific intervention of IRI-induced AKI.
Keywords: Complement activation, Ischemia-reperfusion injury, Kidney, Properdin, Tissue repair, Acute kidney injury.
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