ArticleScientific reports2021
A potent truncated form of human soluble CR1 is protective in a mouse model of renal ischemia-reperfusion injury.
Article in Scientific reports, 2021. 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, 13 citations in OpenAlex.
- In vivo evidence of effective complement modulation by TriFu in comparison to C5 inhibition and complement depletion.Blood advances · 2026Article
- The anti-interleukin-6 antibody ALD518-P18 mitigates murine kidney ischemia-reperfusion injury.Scientific reports · 2026Article
- Targeting the complement lectin pathway with a highly specific MASP-2 inhibitor protects against renal ischemia-reperfusion injury.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Complement activation in wasp venom-induced acute kidney injury.Renal failure · 2024Article
- The Molecular Mechanisms of Complement Receptor 1-It Is Complicated.Biomolecules · 2023Review
- IL-1β-dependent extravasation of preexisting lung-restricted autoantibodies during lung transplantation activates complement and mediates primary graft dysfunction.The Journal of clinical investigation · 2022Article
- Complement-targeting therapeutics for ischemia-reperfusion injury in transplantation and the potential forFrontiers in immunology · 2022Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The complement system is a potent mediator of ischemia-reperfusion injury (IRI), which detrimentally affects the function and survival of transplanted kidneys. Human complement receptor 1 (HuCR1) is an integral membrane protein that inhibits complement activation by blocking the convertases that activate C3 and C5. We have previously reported that CSL040, a truncated form of recombinant soluble HuCR1 (sHuCR1), has enhanced complement inhibitory activity and improved pharmacokinetic properties compared to the parent molecule. Here, we compared the capacity of CSL040 and full-length sHuCR1 to suppress complement-mediated organ damage in a mouse model of warm renal IRI. Mice were treated with two doses of CSL040 or sHuCR1, given 1 h prior to 22 min unilateral renal ischemia and again 3 h later. 24 h after reperfusion, mice treated with CSL040 were protected against warm renal IRI in a dose-dependent manner, with the highest dose of 60 mg/kg significantly reducing renal dysfunction, tubular injury, complement activation, endothelial damage, and leukocyte infiltration. In contrast, treatment with sHuCR1 at a molar equivalent dose to 60 mg/kg CSL040 did not confer significant protection. Our results identify CSL040 as a promising therapeutic candidate to attenuate renal IRI and demonstrate its superior efficacy over full-length sHuCR1 in vivo.
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