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. 2024 Jun 21;11:40. doi: 10.1186/s40779-024-00544-5

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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. 3 — Fibroblast growth factors (FGFs) in intervertebral disc degeneration (IVDD). FGF2 promotes the catabolism of AF, NP, and CEP through FGFR1, and fibrosis of IVD cartilage. FGF2 works through FGFR3 to activate downstream Ras-MAPK and PI3K-Akt signaling pathways to promote anabolism and cell differentiation in various tissues of IVDs. FGF18 promotes tissue synthesis and apoptosis via FGFR3. AF annulus fibrosus, NP nucleus pulposus, CEP cartilaginous endplate, ERK extracellular signal-regulated kinase, MAPK mitogen-activated protein kinase, HS heparan sulfates, FRS2α FGFR substrates 2α, SOS son of sevenless, GRB guanine nucleotide exchange factor, GAB GRB2-associated binding protein, PI3K phosphoinositide 3-kinase, Akt protein kinase B