ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Mannan-binding lectin-associated serine protease 2 is critical for the development of renal ischemia reperfusion injury and mediates tissue injury in the absence of complement C4.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Guiding pluripotent stem cell therapies past the immune system.Stem cells translational medicine · 2026Review
- Collectin-11 regulates osteoclastogenesis and bone maintenance via a complement-dependent mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rationale for Targeting Complement to Mitigate Renal Transplant Ischemia-Reperfusion Injury.Journal of the American Society of Nephrology : JASN · 2026Review
- Multiomics reveal plasma constituents associated with thrombosis among trauma patients who do not respond to enoxaparin.Blood vessels, thrombosis & hemostasis · 2025Article
- Transcriptome analysis of five-toed jerboa organs reveals high-altitude adaptation mechanisms.BMC genomics · 2025Article
- 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
- Complement activation by IgM autoantibodies linked to immune-mediated neuropathies depends on C2.European journal of neurology · 2025Article
- Characterization of a Long-Acting Anti-Human MASP-2 Antibody for the Treatment of Complement-Related Diseases.Journal of inflammation research · 2025Article
- Identification of Endothelial Cell Protein C Receptor by Urinary Proteomics as Novel Prognostic Marker in Non-Recovery Kidney Injury.International journal of molecular sciences · 2024Article
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
- Urinary complement biomarkers in immune-mediated kidney diseases.Frontiers in immunology · 2024Review
- Complement System and the Kidney: Its Role in Renal Diseases, Kidney Transplantation and Renal Cell Carcinoma.International journal of molecular sciences · 2023Review
- Protective effect of IAXO-102 on renal ischemia-reperfusion injury in rats.Journal of medicine and life · 2023Article
- The Complement System in Kidney Transplantation.Cells · 2023Review
- Development and characterization of narsoplimab, a selective MASP-2 inhibitor, for the treatment of lectin-pathway-mediated disorders.Frontiers in immunology · 2023Article
- Complement Inhibition in Kidney Transplantation: Where Are We Now?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Review
- MASP-2 and MASP-3 inhibitors block complement activation, inflammation, and microvascular stasis in a murine model of vaso-occlusion in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2022Article
- Targeting thromboinflammation in COVID-19 - A narrative review of the potential of C1 inhibitor to prevent disease progression.Molecular immunology · 2022Review
- Mannan-binding lectin serine protease-2 (MASP-2) in human kidney and its relevance for proteolytic activation of the epithelial sodium channel.Scientific reports · 2022Article
- Directed Evolution-Driven Increase of Structural Plasticity Is a Prerequisite for Binding the Complement Lectin Pathway Blocking MASP-Inhibitor Peptides.ACS chemical biology · 2022Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
Mannan-binding lectin-associated serine protease 2 (MASP-2) has been described as the essential enzyme for the lectin pathway (LP) of complement activation. Since there is strong published evidence indicating that complement activation via the LP critically contributes to ischemia reperfusion (IR) injury, we assessed the effect of MASP-2 deficiency in an isogenic mouse model of renal transplantation. The experimental transplantation model used included nephrectomy of the remaining native kidney at d 5 post-transplantation. While wild-type (WT) kidneys grafted into WT recipients (n=7) developed acute renal failure (control group), WT grafts transplanted into MASP-2-deficient recipients (n=7) showed significantly better kidney function, less C3 deposition, and less IR injury. In the absence of donor or recipient complement C4 (n=7), the WT to WT phenotype was preserved, indicating that the MASP-2-mediated damage was independent of C4 activation. This C4-bypass MASP-2 activity was confirmed in mice deficient for both MASP-2 and C4 (n=7), where the protection from postoperative acute renal failure was no greater than in mice with MASP-2 deficiency alone. Our study highlights the role of LP activation in renal IR injury and indicates that injury occurs through MASP-2-dependent activation events independent of C4.
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