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ARID5B‐mediated LINC01128 epigenetically activated pyroptosis and apoptosis by promoting the formation of the BTF3/STAT3 complex in β2GPI/anti‐β2GPI‐treated monocytes

Clinical and Translational Medicine 2024 6 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.

Yuan Tan, Yuan Tan, Jiao Qiao, Shuo Yang, Qingchen Wang, Hongchao Liu, Qi Liu, Weimin Feng, Boxin Yang, Boxin Yang, Zhongxin Li, Liyan Cui

Summary

Researchers identified how a protein called ARID5B activates a genetic pathway that triggers cell death through pyroptosis and apoptosis in monocytes associated with antiphospholipid syndrome. They found that ARID5B drives expression of a long non-coding RNA that promotes inflammatory cell death via a specific protein complex. The study suggests that targeting this pathway could offer a potential therapeutic approach for managing this autoimmune condition.

Body Systems

Immune

Models

Human

Study Type In vivo

The H3K4me3 mark and chromatin accessibility at the ARID5B promoter are increased in vitro model mimicked APS. ARID5B-mediated LINC01128 induces pyroptosis and apoptosis via p-STAT3 by binding to BTF3. ARID5B is high- expressed in patients with primary APS and positively correlated with LINC01128 expression. OICR-9429 treatment mitigates pyroptosis and related inflammation in vivo and in vitro models mimicked APS.

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