ArticleCellular and molecular life sciences : CMLS2023
Knockout of the C3a receptor protects against renal ischemia reperfusion injury by reduction of NETs formation.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 24 citations in OpenAlex.
- Salvianolic acid C alleviates acute kidney injury by restoring fructose-1,6-bisphosphatase 1-mediated gluconeogenesis.Renal failure · 2026Article
- Fibrinogen-like protein 2-complement C3 interaction exacerbates tubular inflammation in acute kidney injury by elevating complement C3a levels.Renal failure · 2026Article
- Neutrophil plasticity in inflammation resolution: mechanisms and therapeutic potential.Human cell · 2026Review
- Review
- Review
- C3aR inhibition alleviates cerebral ischemia-reperfusion injury via STING-mediated ferroptosis through SLC7A11/GPX4.iScience · 2026Article
- Effect of complement 3/5 knockout on renal proteomics landscape after ischemia and reperfusion injury in rats.Physiological reports · 2026Article
- Review
- Liver-Targeted Gallium-Polyphenol Network by Disrupting the ROS/NETs/PANoptosis Axis for Precision Acute Liver Injury Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Macrophage C3aR1 Mediates Sepsis-Induced Myocardial Injury by Triggering Neutrophil Necroptosis.Journal of cellular and molecular medicine · 2026Article
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Targeting the Toll-Like Receptor 4 Ameliorates Heart Failure in Aged Mice by Inhibiting the Formation of Neutrophil Extracellular Traps.Physiological research · 2026Article
- Overexpression of Soluble Fibrinogen-like Protein 2 in MSCs Ameliorates Renal Ischemia-Reperfusion Injury in Mice by Modulating Neutrophils.Balkan medical journal · 2026Article
- Interleukin-33 Promotes Neutrophil Extracellular Trap Formation To Aggravate Renal Ischemia-Reperfusion Injury Through ST2/PI3K/Akt and ST2/PAD4 Pathways.Inflammation · 2026Article
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- The Current Application Prospects of Nanomedicine in Renal Ischemia-Reperfusion Injury.International journal of nanomedicine · 2026Review
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Study on the pro-inflammatory injury of neutrophil extracellular traps in gouty nephropathy.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Renal ischemia/reperfusion (I/R) injury is a local sterile inflammatory response driven by innate immunity. Emerging data have revealed that complement and neutrophils contribute to hyperinflammation and oxidative stress in I/R induced acute kidney injury (AKI). However, the interplay between the C3a/C3aR axis and neutrophil extracellular traps (NETs) is imcompletelyunderstood. Here, we utilize genetically engineered mouse models and pharmacological inhibitors to investigate this association. The C3a/C3aR axis is found to promote neutrophil recruitment and NETs formation, thereby accelerating renal damage and dysfunction. Knockout of C3aR restores NETs release and improves renal function after I/R injury. Antibody-mediated blockade of NETs can also significantly ameliorate renal tubular injury and inflammation. Consistently, under stimulation by C3a, neutrophils are activated to promote NETs formation and subsequent renal tubular epithelial cell damage, and blocking C3aR rescued the injury. Interfering with reactive oxygen species (ROS) accumulation in neutrophils by antioxidant treatment significantly attenuates NETs formation. Our findings demonstrate that the C3a/C3aR-ROS-NETs axis constitutes a promising target for prevention or treatment of renal I/R injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.