ArticleBiology2026
Pharmacological TLR4 Activation Promotes Hepatocyte Proliferation and Liver Repair Through Coordinated IL-6 and TCDCA Signaling.
Article in Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
The regenerative capacity of the liver is frequently insufficient following severe injury, and effective therapeutic strategies remain limited. Here, we identify CRX-527, a TLR4 agonist, as a novel inducer of hepatocyte proliferation in both healthy mice and a model of acetaminophen (APAP)-induced acute liver injury. Immunofluorescence analysis revealed that CRX-527-induced proliferative activity was predominantly observed in zone 2. Mechanistically, CRX-527 acts via TLR4 to induce transient IL-6 secretion, which subsequently activates the JAK2/STAT3 signaling pathway. In addition, metabolomic profiling identified taurochenodeoxycholic acid (TCDCA) as a synergistic partner of IL-6 in promoting hepatocyte proliferation. In APAP-injured mice, treatment with CRX-527 alone or in combination with IL-6 and TCDCA significantly reduced hepatic necrosis, accelerated tissue repair, and improved survival. Collectively, our findings uncover a previously unrecognized combined effect between IL-6/JAK2/STAT3 signaling and TCDCA in promoting hepatocyte proliferation and highlight CRX-527 and the IL-6/TCDCA combination as potential regenerative targets that warrant further preclinical evaluation for drug-induced liver injury, particularly in the setting of APAP overdose.
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