ArticleNature communications2025
Myeloid EGFR deficiency accelerates recovery from AKI via macrophage efferocytosis and neutrophil apoptosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A tri-scale in silico framework integrating pharmacovigilance and mechanistic modeling suggests tepotinib-associated acute kidney injury risk.Renal failure · 2026Article
- Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026Review
- EGFR orchestrates neutrophil activation and NETosis via CEBPβ-dependent PGLYRP1 induction.Cell death and differentiation · 2026Article
- A study on the association between polycyclic aromatic hydrocarbon (PAH) exposure and kidney function indicators in adolescents: an integrated research combining statistical mediation analysis and network toxicology.International urology and nephrology · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Neutrophil-Driven Cascade-Targeted Nanocarriers Restore Mitochondrial Homeostasis to Ameliorate Renal Ischemia-Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Network Toxicology Reveals the Mechanisms of the Plasticizer Metabolite MECPP in Metabolic Diseases.International journal of molecular sciences · 2026Article
- The ErbB-tyrosine kinase inhibitor, neratinib, has anti-inflammatory effects in multimorbidity by increasing macrophage efferocytosis via the upregulation of MerTK.Journal of inflammation (London, England) · 2026Article
- Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025Review
- Neutrophil and neutrophil extracellular traps in acute kidney injury: from mechanisms to treatments.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Altered expression and activation of Epidermal Growth Factor Receptor (EGFR) is implicated in acute and chronic kidney injury. One of the important cellular sources of EGFR is the myeloid compartment, which plays roles in both acute kidney injury and subsequent fibrosis. Here we show in a murine ischemic acute kidney injury (AKI) model that myeloid deletion of EGFR promotes a pro-resolving, anti-inflammatory phenotype and increased efferocytotic capacity in macrophages. This leads to accelerated recovery in response to AKI and inhibited subsequent development of tubulointerstitial fibrosis. We find that selective EGFR deletion in neutrophils also accelerates recovery from ischemic kidney injury and reduces subsequent fibrosis. EGFR activation plays an essential role in increasing the life span of neutrophils in the injured kidney. Deletion of EGFR expression either in all murine myeloid cells or selectively in neutrophils decreases kidney neutrophil Mcl-1 expression and promotes neutrophil apoptosis, which is accompanied by accelerated recovery from organ injury and reduced subsequent fibrosis. These studies thus identify coordinated and complementary roles for EGFR activation in neutrophils and macrophages to exacerbate kidney injury.
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