Metabolic Checkpoints in Rheumatoid Arthritis: SARM1-Mediated PANoptosis Sustains Autoimmune Tissue Inflammation
Audience: Member of University - ALL Format: In PersonMonday, 8 June 2026, 12pm to 1pm
Chronic inflammation in autoimmune disease reflects a failure to resolve immune responses despite the presence of tissue-repair programs. Emerging evidence points to metabolic checkpoints as key determinants of immune cell fate, linking cellular bioenergetics to inflammatory function and survival. In rheumatoid arthritis, reparative macrophages undergo a metabolic shift driven by autocrine C1q signaling, leading to activation of the NAD⁺ hydrolase SARM1. This results in NAD⁺ depletion, mitochondrial crisis, and accumulation of cyclic ADP ribose, which triggers PANoptotic cell death. The resulting lytic death amplifies tissue inflammation, identifying SARM1-dependent metabolic collapse as a mechanism sustaining chronic autoimmune pathology and a potential therapeutic target.
Speaker(s): Prof. Cornelia Weyand (Mayo Clinic College of Medicine and Science and the Mayo Clinic Alix School of Medicine)
Venue:
Kennedy Institute of Rheumatology - Kennedy Lecture Theatre
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Kennedy Lecture Theatre Kennedy Institute of Rheumatology Headington Oxford Oxfordshire OX3 7FY United Kingdom
Department: Kennedy Institute of Rheumatology (Unit)
Organiser: Tess Lawless
Host: Professor Christopher Buckley
