Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Mar 24;7:95. doi: 10.1038/s41392-022-00934-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

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/.

PMC Copyright notice

Fig. 3 — The role of NOTCH signaling in body development and damage repair. NOTCH signaling is involved in regulating the differentiation and function of stem cells, affecting organ production and damage repair. a NOTCH signaling promotes the self-renewal of stem cells, induces multipotent progenitors for lineage selection, and generates different terminal cells; when the organ is damaged, cell type A is damaged and destroyed, and the stimulated cell type B rapidly upregulates the expression of NOTCH signaling to promote their own proliferation, and is partially redifferentiated into cell type A. b Highly activated NOTCH induces the expression of bile duct cell-enriched transcription factors and promotes the differentiation of multipotent hepatocyte progenitors into bile duct epithelial cells. c In liver injury, BEC are damaged and destroyed. NOTCH signaling is highly expressed in hepatocytes, which are further transformed into biphenotypic cells, which manifests the biliary tract morphology, and finally generate new BEC (BEC’) to form small tubular structures. HPC, hematopoietic progenitor cell; BEC, bile duct epithelial cell; SOX9, SRY-related high-mobility group box 9; HNF, hepatocyte nuclear factor