Crosstalk between macrophages and adjacent cells in AKI to CKD transition

Acute kidney injury (AKI), triggered by ischemia, sepsis, toxicity, or obstruction, is marked by a rapid impairment of renal function and could lead to the initiation and advancement of chronic kidney disease (CKD). The concept of AKI to CKD transition has gained much interest. Despite a series of s...

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Bibliographic Details
Published inRenal failure Vol. 47; no. 1; p. 2478482
Main Authors Lin, Yanping, Yang, Qian, Zeng, Rui
Format Journal Article
LanguageEnglish
Published England Taylor & Francis Group 01.12.2025
Subjects
Acute kidney injury
Acute Kidney Injury - complications
Acute Kidney Injury - immunology
Acute Kidney Injury - pathology
AKI to CKD transition
Animals
Cell Communication - immunology
Chronic kidney disease
Disease Progression
Endothelial Cells
Epithelial Cells
Humans
Intercellular communication
Macrophages
Macrophages - immunology
Macrophages - metabolism
Renal Insufficiency, Chronic - etiology
Renal Insufficiency, Chronic - immunology
Renal Insufficiency, Chronic - pathology
AKI to CKD transition
Chronic kidney disease
Macrophages
Acute kidney injury
Intercellular communication
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Summary:Acute kidney injury (AKI), triggered by ischemia, sepsis, toxicity, or obstruction, is marked by a rapid impairment of renal function and could lead to the initiation and advancement of chronic kidney disease (CKD). The concept of AKI to CKD transition has gained much interest. Despite a series of studies highlighting the diverse roles of renal macrophages in the immune response following AKI, the intricate mechanisms of macrophage-driven cell-cell communication in AKI to CKD transition remains incompletely understood. In this review, we introduce the dynamic phenotype change of macrophages under the different stages of kidney injury. Importantly, we present novel perspectives on the extensive interaction of renal macrophages with adjacent cells, including tubular epithelial cells, vascular endothelial cells, fibroblasts, and other immune cells via soluble factors, extracellular vesicles, and direct contact, to facilitate the transition from AKI to CKD. Additionally, we summarize the potential therapeutic strategies based on the adverse macrophage-neighboring cell crosstalk.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ObjectType-Review-3
content type line 23
ISSN:0886-022X
1525-6049
1525-6049
DOI:10.1080/0886022X.2025.2478482