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. 2020 Sep 25;11(9):802. doi: 10.1038/s41419-020-03003-w

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — In healthy liver, different hepatic cell types such as hepatocytes, KCs, HSCs and LSECs, communicate and regulate each other by secreting signalling mediators. Upon NAFLD condition, after FFAs overload, damaged cells release higher amounts of pro-inflammatory cytokines, damage-associated patterns (DAMPs), extracellular vesicles (EVs) and other molecules that can activate HSCs and KCs and promote LSECs to lose their fenestrations, likely contributing in a coordinated manner to the progression of NASH to more severe stages of NAFLD.