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. 2024 Mar 27;628(8008):604–611. doi: 10.1038/s41586-024-07237-y

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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/.

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Extended Data Fig. 10 — The schematic shows the proposed mechanisms by which nociceptors promote tissue healing via controlling neutrophils and monocytes/macrophages (Mo/Mϕ) in injured tissues. Following tissue injury, CGRP-expressing nociceptor endings grow into the granulation tissue. CGRP signalling in neutrophils and macrophages induces the release of the ECM protein TSP-1. TSP-1 is deposited in the injured tissue milieu inhibiting neutrophil and monocytes/macrophage migration and eventually accelerating the cell death response of neutrophils and macrophages to inflammatory cytokines. In addition, CGRP promotes efferocytosis and macrophage polarization into a M2-like phenotype via an autocrine or paracrine effect of TSP-1. Overall, nociceptors are critical for the transition of the injured tissue microenvironment towards a tissue healing phase. Blue line indicates inhibition, red line indicates induction. Dashed grey lines indicate that CGRP and TSP-1 may also promote tissue healing by acting on non-immune cells. Created with BioRender.com.