ArticleThe Journal of experimental medicine2014
Dissecting the complement pathway in hepatic injury and regeneration with a novel protective strategy.
Article in The Journal of experimental medicine, 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, 88 citations in OpenAlex.
- Perioperative gut microbial ecology: a new frontier for improving the prognosis of hepatocellular carcinoma surgery.Precision clinical medicine · 2026Review
- Integration of multiomic and multi-phenotypic data identifies biological pathways associated with physical fitness.Communications biology · 2026Article
- Therapeutic Potential of C1-Inhibitor in Vascular Diseases and Beyond.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Therapeutic priming of liver regeneration: from mechanisms toFrontiers in transplantation · 2026Review
- Quercetin Ameliorates Skeletal Muscle Fibrosis After Injury by Interfering with Macrophage-Myofibroblast Transition.Journal of inflammation research · 2026Article
- Immunogenicity Management Strategies for PEGylated Drug Delivery Systems.International journal of nanomedicine · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells.Cellular & molecular immunology · 2025Review
- Role of local complement activation in kidney fibrosis and repair.The Journal of clinical investigation · 2025Review
- Research progress on the roles of complement in liver injury.World journal of hepatology · 2025Review
- A Newly Identified Protective Role of C5a Receptor 1 in Kidney Tubules against Toxin-Induced Acute Kidney Injury.The American journal of pathology · 2025Article
- Macrophage-Myofibroblast Transition as a Potential Origin for Skeletal Muscle Fibrosis After Injury via Complement System Activation.Journal of inflammation research · 2024Article
- Current progress on the microbial therapies for acute liver failure.Frontiers in microbiology · 2024Review
- Modulation of the hepatic RANK-RANKL-OPG axis by combined C5 and CD14 inhibition in a long-term polytrauma model.Frontiers in immunology · 2024Article
- The role of ischaemia-reperfusion injury and liver regeneration in hepatic tumour recurrence.JHEP reports : innovation in hepatology · 2023Review
- Article
- Liver FoxO1 overexpression is positively associated with the degree of liver injury in cirrhotic patients.Advances in laboratory medicine · 2023Article
- Properdin inhibition ameliorates hepatic ischemia/reperfusion injury without interfering with liver regeneration in mice.Frontiers in immunology · 2023Article
- Analysis and identification of potential key genes in hepatic ischemia-reperfusion injury.Annals of translational medicine · 2022Article
- Overexpression of miR-125a-5p Inhibits Hepatocyte Proliferation through the STAT3 Regulation In Vivo and In Vitro.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Liver resection is commonly performed under ischemic conditions, resulting in two types of insult to the remnant liver: ischemia reperfusion injury (IRI) and loss of liver mass. Complement inhibition is recognized as a potential therapeutic modality for IRI, but early complement activation products are also essential for liver regeneration. We describe a novel site-targeted murine complement inhibitor, CR2-CD59, which specifically inhibits the terminal membrane attack complex (MAC), and we use this protein to investigate the complement-dependent balance between liver injury and regeneration in a clinical setting of pharmacological inhibition. CR2-CD59 did not impact in vivo generation of C3 and C5 activation products but was as effective as the C3 activation inhibitor CR2-Crry at ameliorating hepatic IRI, indicating that the MAC is the principle mediator of hepatic IRI. Furthermore, unlike C3 or C5 inhibition, CR2-CD59 was not only protective but significantly enhanced hepatocyte proliferation after partial hepatectomy, including when combined with ischemia and reperfusion. Remarkably, CR2-CD59 also enhanced regeneration after 90% hepatectomy and improved long-term survival from 0 to 70%. CR2-CD59 functioned by increasing hepatic TNF and IL-6 levels with associated STAT3 and Akt activation, and by preventing mitochondrial depolarization and allowing recovery of ATP stores.
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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.