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. 2022 Aug 10;11(8):561–574. doi: 10.1302/2046-3758.118.BJR-2021-0576.R1

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© 2022 Author(s) et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (CC BY-NC-ND 4.0) licence, which permits the copying and redistribution of the work only, and provided the original author and source are credited. See https://creativecommons.org/licenses/by-nc-nd/4.0/

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Fig. 3 — Role of Janus kinase signal transducer and activator of transcription (JAK/STAT) and bone morphogenetic protein (BMP) pathways in tendon healing and degeneration. Simplified scheme of selected signalling pathways involved in tendon healing. The balance of M1 and M2 macrophage polarization plays a central role in resolving the inflammatory phase and affects the outcome of tendon healing. Proinflammatory cytokines released during dominant and prolonged M1 macrophage polarization stimulate molecular factors released in response of the JAK/STAT pathway activation, which can trigger the senescence-associated secretory phenotype (SASP) shift of tendon cells. SASP is associated with degenerative features in healing tendons. Mediators released during M2 macrophage polarization, including anti-inflammatory cytokines such as interleukin (IL)-10, stimulate other parts of the JAK/STAT pathway. Proteoglycans such as biglycan and fibromodulin can bind and stabilize growth factors activating the BMP pathway. Tenomodulin produced by the tendon cells can exert pro-proliferative effect as well as protective roles against cellular senescence and unrestrained angiogenesis. The image was created by G. G. Schulze-Tanzil using Krita 4.1.7 (Krita Foundation, The Netherlands). β-gal, β-galactosidase; ECM, extracellular matrix; IFNγ, interferon γ; MMP, matrix metalloproteinase; ROS, reactive oxygen species; TGFβ, transforming growth factor β; TNMD, tenomodulin.