Toxic lipid-induced epigenetic activation of ICAM1 in liver sinusoidal endothelium regulates myeloid-driven fibro-inflammatory response in MASH

Qianqian Guo; Nantawat Satthawiwat; Akitoshi Sano; Chady Meroueh; Asma Hamdi; 戴新; Khaled Warasnhe; Alexander M. Washington; Patrick P. Starlinger; Alex Krivonos; Sheng Cao; Enis Kostallari; Johan W. Jonker; Bart van de Sluis; Feda H. Hamdan; Samar H. Ibrahim

doi:10.1097/hep.0000000000001742

April 15, 2026Hepatology

Toxic lipid-induced epigenetic activation of ICAM1 in liver sinusoidal endothelium regulates myeloid-driven fibro-inflammatory response in MASH

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Key Points

The research aims to investigate the role of epigenetic changes in ICAM1 expression during lipotoxic stress in liver sinusoidal endothelial cells.
Analyzed ICAM1 expression in liver sinusoidal endothelial cells under lipotoxic conditions.
Assessed myeloid cell recruitment in a MASH model.
Evaluated potential epigenetic modifications affecting ICAM1.
ICAM1 expression was significantly increased in liver sinusoidal endothelial cells during lipotoxic stress.
Enhanced recruitment of myeloid cells was observed in MASH models.
Targeting ICAM1's epigenetic regulation might serve as a therapeutic approach for MASH.

Implication

Uncovers how toxic lipids activate ICAM1 in liver cells, indicating a potential treatment for MASH.

Abstract

ICAM1 is epigenetically upregulated in LSECs during lipotoxic stress and promotes myeloid cell recruitment in MASH. Targeting the epigenetic regulation of ICAM1 may offer a novel therapeutic strategy for treating human MASH.

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Cite This Study

Guo et al. (2026) studied this question.

synapsesocial.com/papers/69e1cf625cdc762e9d85843b https://doi.org/10.1097/hep.0000000000001742

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Toxic lipid-induced epigenetic activation of ICAM1 in liver sinusoidal endothelium regulates myeloid-driven fibro-inflammatory response in MASH

Key Points

Implication

Abstract

Discussion

Cite This Study

Toxic lipid-induced epigenetic activation of ICAM1 in liver sinusoidal endothelium regulates myeloid-driven fibro-inflammatory response in MASH

Key Points

Implication

Abstract

Discussion

Cite This Study

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