ArticleInflammation2025
Mac-1 Promotes Neutrophil Extracellular Traps Formation via ERK Phosphorylation in Renal Ischemia-Reperfusion Injury.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Targeting iRhom2-mediated PANoptosis ameliorates acute kidney injury.Acta pharmacologica Sinica · 2026Article
- Review
- Neutrophils and Neutrophil Extracellular Traps in Hepatic Ischemia-Reperfusion Injury: Molecular Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Perioperative neutrophil-to-lymphocyte ratio trajectories and creatinine-defined acute kidney disease after cardiac surgery: a study using the INSPIRE database.Frontiers in cardiovascular medicine · 2026Article
- Neutrophils in Kidney Disease: Linking Neutrophil Function and Microenvironment to Therapeutic Targets.Journal of inflammation research · 2026Review
- Neutrophil-mediated myocardial ischemia-reperfusion injury: mechanisms and potential therapeutic targets.Frontiers in immunology · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in the animal model of adenine-induced chronic kidney disease.PloS one · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
Neutrophils are key effector cells in the pathogenesis of acute kidney injury (AKI), where neutrophil extracellular traps (NETs) play a critical role. Mac-1 (CD11b/CD18), a leukocyte surface integrin, is known to mediate inflammation. We hypothesized that Mac-1 regulates NETs formation and exacerbates ischemic AKI. The expression of Mac-1 and NETs was analyzed in peripheral blood and renal tissues from patients with kidney diseases. Mac-1 knockout (Mac-1⁻/⁻) mice were used to establish a bilateral renal ischemia-reperfusion injury (IRI) model and compared with wild-type (WT) controls. Primary neutrophils were isolated from bone marrow in vitro to investigate the mechanisms underlying NETs formation. CD11b and NETs were both implicated in patients with either AKI following cardiac surgery or interstitial nephritis. In a murine bilateral renal IRI model, NETs formation was detected in WT kidneys at 24 h, and DNase I treatment significantly alleviated renal injury. Compared to WT mice, Mac-1⁻/⁻ mice exhibited reduced dysfunction, inflammation, and NETs infiltration. In vitro, Mac-1⁻/⁻ neutrophils showed decreased PMA-induced NETs formation and reduced ERK phosphorylation. Furthermore, treatment with anti-Mac-1 antibody (M1/70) in the murine IRI model significantly attenuated kidney inflammation and injury. Mac-1 exacerbates kidney inflammation and dysfunction in ischemic AKI by mediating NETs formation through an ERK phosphorylation-dependent mechanism. Blockade of Mac-1 using the antibody M1/70 effectively ameliorates this injury, highlighting its potential as a therapeutic target.
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