Abstract
Acute kidney injury (AKI) is a common and devastating clinical condition with a high morbidity and mortality rate and is associated with a rapid decline of kidney function mostly resulting from the injury of proximal tubules. AKI is typically accompanied by inflammation and immune activation and involves macrophages (Mϕ) from the beginning: The inflamed kidney recruits “classically” activated (M1) Mϕ, which are initially poised to destroy potential pathogens, exacerbating inflammation. Of note, they soon turn into “alternatively” activated (M2) Mϕ and promote immunosuppression and tissue regeneration. Based on their roles in kidney recovery, there is a growing interest to use M2 Mϕ and Mϕ-modulating agents therapeutically against AKI. However, it is pertinent to note that the clinical translation of Mϕ-based therapies needs to be critically reviewed and questioned since Mϕ are functionally plastic with versatile roles in AKI and some Mϕ functions are detrimental to the kidney during AKI. In this review, we discuss the current state of knowledge on the biology of different Mϕ subtypes during AKI and, especially, on their role in AKI and assess the impact of versatile Mϕ functions on AKI based on the findings from translational AKI studies.
Highlights
Severe Acute kidney injury (AKI) is a clinical condition closely linked with a high morbidity and mortality rate (Zuk and Bonventre, 2016)
This review has provided insights into the net effect of versatile Mφ functions in AKI by Mφ removal studies (Figure 1)
Several studies suggest that the depletion of global Mφ in AKI can be beneficial to the injury kidney
Summary
Severe AKI is a clinical condition closely linked with a high morbidity and mortality rate (Zuk and Bonventre, 2016). AKI mostly results from the injury of proximal tubules and is accompanied by inflammation and immune activation (Zuk and Bonventre, 2019). Versatile Mφ Functions in AKI a role in the transition of AKI to CKD. Whilst valuing its immense therapeutic potential, it is to acknowledge that the clinical translation of Mφ-based therapies needs to be critically reviewed and questioned, especially since Mφ act like doubleedged swords being both beneficial and harmful to the injured tissue (Figure 1) (Braga et al, 2015). We discuss the current state of knowledge on the biology of different Mφ subtypes during AKI and on the impact of global Mφ and Mφ subtypes on AKI based on the findings from in vivo Mφ depletion studies. We outline Mφ-based therapeutic strategies for the treatment of AKI
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