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. 2021 Mar 21;24(2):289–310. doi: 10.1007/s10456-021-09780-y

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© The Author(s) 2021

Open AccessThis 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/.

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Fig. 6 — Angiocrine control of liver regeneration. Angiocrine signaling is indispensable for liver regeneration. a During the early inductive phase of liver regeneration, downregulation of EC ANGPT2 leads to downregulation of TGF-β production, thereby facilitating hepatocyte proliferation. During the later angiogenic phase, EC ANGPT2 production rebounds to control LSEC proliferation by regulating VEGFR2 in an autocrine Tie2-dependent manner in response to hepatocyte-derived VEGF. EC ANGPT2 thereby serves as a spatiotemporally regulated rheostat dynamically controlling regenerating hepatocytes and angiogenic EC. b The balance between pro-regenerative (CXCR7-Id1) and pro-fibrotic (CXCR4) pathways modulates liver regeneration. The pro-regenerative CXCR7-Id1 pathway is upregulated during liver regeneration, to induce Wnt2 and HGF. In addition to CXCR7, the VEGFR2-Id1-mediated pathway triggers the angiocrine factors Wnt2 and HGF to boost hepatocyte proliferation. c Activated platelets from the injured area release stromal-derived factor-1 (SDF1) to activate pro-regenerative CXCR7-mediated signaling. d Angiocrine HGF can be induced by blood perfusion-regulated mechano-sensing mechanisms. Increased blood flow resulting from hepatic injury upregulates VEGFR3 and β1-integrins for HGF production