Shanghai Institute of Materia Medica's Bo Shan details how metabolic signals control immune cell phenotypes
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Dr. Bo Shan of the Shanghai Institute of Materia Medica delivered a lecture on how metabolic signals regulate immune cell phenotypes, connecting fat browning with liver regeneration. In fat tissue, his team found that deleting the mitochondrial protein LUMP1 in adipocytes blocks cold-induced browning by degrading SDHB and stabilizing succinate, which shifts the succinate/α-KG ratio and alters histone methylation. In the liver, a CD36-positive monocyte-derived macrophage subpopulation takes up lipids, activating the IRE1-XBP1 pathway to raise IL-6 and drive hepatocyte proliferation; IL-6 rescue restores proliferation when CD36 or IRE1 is knocked out. The lecture, presented on October 14, 2026, laid out the mechanistic work but left open questions such as how these pathways might translate into therapeutic targets.
Written by a model from the reports · updated 2 hours ago
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Dr. Shan of the Shanghai Institute of Materia Medica gave a lecture on how metabolic signals regulate immune cell phenotypes, linking fat browning and liver regeneration. His team found that deleting the mitochondrial protein LUMP1 in adipocytes blocks cold-induced browning by degrading SDHB and stabilizing succinate, which alters the succinate/α-KG ratio and histone methylation. In liver regeneration, a CD36-positive monocyte-derived macrophage subpopulation takes up lipids, activating the IRE1-XBP1 pathway to raise IL-6 and drive hepatocyte proliferation, with IL-6 rescue restoring proliferation when CD36 or IRE1 is knocked out.
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