Abstract
Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), which contributes to the development of chronic kidney disease (CKD). Renal IRI combines major events, including a strong inflammatory immune response leading to extensive cell injuries, necrosis and late interstitial fibrosis. Macrophages act as key players in IRI-induced AKI by polarizing into proinflammatory M1 and anti-inflammatory M2 phenotypes. Compelling evidence exists that the stress-responsive enzyme, heme oxygenase-1 (HO-1), mediates protection against renal IRI and modulates macrophage polarization by enhancing a M2 subset. Hereafter, we review the dual effect of macrophages in the pathogenesis of IRI-induced AKI and discuss the critical role of HO-1 expressing macrophages.
Highlights
Macrophages play a critical role in ischemiareperfusion injury (IRI)-induced Acute kidney injury (AKI) by exhibiting distinct phenotypes, which contribute to either inflammation, tissue injury or kidney repair [10]
This review summarizes the dual effect of macrophages on renal IRI and analyzes the role of the heme oxygenase-1 (HO-1) cytoprotective pathway as an emerging target for understanding the macrophage phenotypic switch
Due to high expression of adhesion-related receptor CX3CR1, this monocyte subset exhibits the ability to patrol in the bloodstream and migrates to healthy tissues where they differentiate into resident macrophages and dendritic cells (DCs) [32,33,34]
Summary
The pathophysiology of IRI-induced AKI is very complex and combines major ischemia-induced cell stress, a significant burst of free radicals, and strong inflammatory immune responses leading to extensive cell injury, tissue damage, and subsequent kidney dysfunction [3,8,9]. In this context, macrophages play a critical role in IRI-induced AKI by exhibiting distinct phenotypes, which contribute to either inflammation, tissue injury or kidney repair [10]. To better understand the impact of macrophages in renal IRI, it is essential to briefly discuss the role of renal tubular epithelial cells (RTECs) and other myeloid cells in the pathogenesis of IRI-induced AKI
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