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. 2024 Jun 28;22:346. doi: 10.1186/s12964-024-01720-9

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Ox-LDL, palmitate, adipokines (TNF-a and IL-6) and LPS lead to inflammatory phenotypes in LSECs, which induce LSECs to produce pro-inflammatory mediators in MASH, including TNF-α, IL-6, IL-1 and CCL2. Lipotoxic stress can enhance the VCAM-1 expression of LSECs through MLK3/P38 signal transduction, and stimulate monocytes to gather in the liver through fenestrae and activate into a pro-inflammatory state. In addition, IL-6 and TNF-α in local microenvironment down-regulate autophagy and increase the expression of CCL2, CCL5, IL-6, Caspase-3, α-SMA and TGF-β1 by inhibiting AMPKα, and activation of Notch signal in damaged LSECs inhibits eNOS transcription, which aggravates liver inflammation and fibrosis, and then promotes the progression of MASH. MOMF: monocyte-derived macrophages