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SUMMARY:Metabolic Checkpoints in Rheumatoid Arthritis: SARM1-Mediated PANo
 ptosis Sustains Autoimmune Tissue Inflammation
DTSTART;TZID=Europe/London:20260608T120000
DTEND;TZID=Europe/London:20260608T130000
DTSTAMP:20260527T012223Z
UID:ad6a7f07-1055-f111-bec6-7ced8d6bf634
CREATED:20260521T122440Z
DESCRIPTION: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 functio
 n 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\, mitocho
 ndrial crisis\, and accumulation of cyclic ADP ribose\, which triggers PAN
 optotic cell death. The resulting lytic death amplifies tissue inflammatio
 n\, identifying SARM1-dependent metabolic collapse as a mechanism sustaini
 ng chronic autoimmune pathology and a potential therapeutic target.
LAST-MODIFIED:20260521T122551Z
LOCATION:Kennedy Institute of Rheumatology - Kennedy Lecture Theatre\, Ken
 nedy Lecture Theatre Kennedy Institute of Rheumatology Headington Oxford O
 xfordshire OX3 7FY United Kingdom
SPEAKER:Prof. Cornelia Weyand (Mayo Clinic College of Medicine and Science
  and the Mayo Clinic Alix School of Medicine)
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