ArticleJACC. Basic to translational science2025
NLRP3 Inflammasome Inhibition by the Novel Bispecific Antibody InflamAb Attenuates Atherosclerosis in Apolipoprotein E-Deficient Mice.
Article in JACC. Basic to translational science, 2025. 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.
- S100A8/A9 and S100A12 Proteins and Macrophage Polarization: Therapeutic Targets in Atherosclerosis.Biomolecules · 2026Review
- Inflammation and Immune Mediators in the Context of Atherosclerotic Cardiovascular Disease and Percutaneous Coronary Intervention: Implications for Therapeutics.Medical sciences (Basel, Switzerland) · 2026Review
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways-A Critical Review.Antioxidants (Basel, Switzerland) · 2026Review
- Costunolide, a Sesquiterpene Lactone, Protects Against Platelet Activation and Thrombus Formation.Cells · 2026Article
- Macrophages in human atherosclerotic plaques in the era of single-cell and spatial transcriptomics.ImmunoHorizons · 2026Review
- Direct NLRP3 inflammasome inhibitors for cardiovascular therapeutics: a comparative review of synthetic and natural candidates.Frontiers in pharmacology · 2026Review
- Temporal Expression of NLRP3 Inflammasome Components in Patients with Acute Coronary Syndrome.Life (Basel, Switzerland) · 2025Article
- Antibody Matrimony in a Duel of Hearts.JACC. Basic to translational science · 2025Article
- The Interplay Between Immunity, Inflammation and Endothelial Dysfunction.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRP3 inflammasome contributes to the inflammatory process in atherosclerosis by producing IL-1β. Components of the intracellular NLRP3 inflammasome have been shown to be expressed by macrophages in the atherosclerotic plaque and are a potential therapeutic target. We aimed to determine the efficacy of the novel bispecific antibody InflamAb, designed to target the interleukin-1 receptor type 1 and the NLRP3 inflammasome, in inhibiting atherosclerosis. InflamAb effectively inhibited IL-1β secretion from bone marrow-derived macrophages and reduced circulating IL-1β levels in vivo. Furthermore, InflamAb treatment significantly inhibited atherosclerotic plaque development, accompanied by a reduction in relative macrophage and necrotic core content. InflamAb treatment did not affect the size of established atherosclerotic lesions; however, InflamAb significantly reduced relative macrophage and necrotic core content in these plaques. To conclude, inhibition of the NLRP3 inflammasome by the bispecific antibody InflamAb shows promising efficacy in inhibiting atherosclerotic plaque development and destabilization in Apoe
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