ArticleInternational journal of molecular sciences2022
Therapeutic Intervention with Anti-Complement Component 5 Antibody Does Not Reduce NASH but Does Attenuate Atherosclerosis and MIF Concentrations in Ldlr-/-.Leiden Mice.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Complement Components C1r and C8 Serve as Potential Inflammatory Biomarkers for Coronary Heart Disease Severity: The Mediating Role of C-Reactive Protein.Journal of inflammation research · 2026Article
- Obesity accelerates age-related memory deficits and alters white matter tract integrity in Ldlr-/-.Leiden mice.Brain, behavior, & immunity - health · 2025Article
- Article
- Canonical and non-canonical roles of complement in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Genetic association with autoimmune diseases identifies molecular mechanisms of coronary artery disease.iScience · 2024Article
- The clinical role of combined circulating complement C1q and AIP for CAD with LDL-C level below 1.8mmol/L.Lipids in health and disease · 2024Article
- Deficiency of Caspase-1 Attenuates HIV-1-Associated Atherogenesis in Mice.International journal of molecular sciences · 2023Article
- Advances in Molecular and Translational Medicine.International journal of molecular sciences · 2023Article
- Article
- Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody.Frontiers in cellular neuroscience · 2023Article
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Authors and funding
16 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic inflammation is an important driver in the progression of non-alcoholic steatohepatitis (NASH) and atherosclerosis. The complement system, one of the first lines of defense in innate immunity, has been implicated in both diseases. However, the potential therapeutic value of complement inhibition in the ongoing disease remains unclear.
methodsAfter 20 weeks of high-fat diet (HFD) feeding, obese Ldlr-/-.Leiden mice were treated twice a week with an established anti-C5 antibody (BB5.1) or vehicle control. A separate group of mice was kept on a chow diet as a healthy reference. After 12 weeks of treatment, NASH was analyzed histopathologically, and genome-wide hepatic gene expression was analyzed by next-generation sequencing and pathway analysis. Atherosclerotic lesion area and severity were quantified histopathologically in the aortic roots.
resultsAnti-C5 treatment considerably reduced complement system activity in plasma and MAC deposition in the liver but did not affect NASH. Anti-C5 did, however, reduce the development of atherosclerosis, limiting the total lesion size and severity independently of an effect on plasma cholesterol but with reductions in oxidized LDL (oxLDL) and macrophage migration inhibitory factor (MIF).
conclusionWe show, for the first time, that treatment with an anti-C5 antibody in advanced stages of NASH is not sufficient to reduce the disease, while therapeutic intervention against established atherosclerosis is beneficial to limit further progression.
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