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Comment
. 2022 Feb 24;14(1):mjab080.
doi: 10.1093/jmcb/mjab080.

Chemokine CCL1 as a therapeutic target for pulmonary fibrosis: comments on 'The chemokine CCL1 triggers an AMFR‒SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis'

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Comment

Chemokine CCL1 as a therapeutic target for pulmonary fibrosis: comments on 'The chemokine CCL1 triggers an AMFR‒SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis'

Shanshan Liu et al. J Mol Cell Biol. .
No abstract available

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Figures

Figure 1
Figure 1
Illustration of the CCL1 working model in pulmonary fibrosis. Chronic lung injury triggers the release of CCL1 from activated alveolar macrophages, and this in turn activates lung fibroblasts by binding to AMFR on the membrane of these cells, thereby driving fibrogenic protein synthesis by activating the Ras‒ERK‒p70S6K pathway. AEC1, type I alveolar epithelial cells; AEC2, type 2 alveolar epithelial cells.

Comment on

References

    1. Chen B., Mariano J., Tsai Y.C.et al. (2006). The activity of a human endoplasmic reticulum-associated degradation E3, gp78, requires its Cue domain, RING finger, and an E2-binding site. Proc. Natl Acad. Sci. USA 103, 341–346. - PMC - PubMed
    1. Gombert M., Dieu-Nosjean M.C., Winterberg F.et al. (2005). CCL1‒CCR8 interactions: an axis mediating the recruitment of T cells and Langerhans-type dendritic cells to sites of atopic skin inflammation. J. Immunol. 174, 5082–5091. - PubMed
    1. Knipfer L., Schulz-Kuhnt A., Kindermann M.et al. (2019). A CCL1/CCR8-dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation. J. Exp. Med. 216, 2763–2777. - PMC - PubMed
    1. Lau S., Feitzinger A., Venkiteswaran G.et al. (2020). A negative-feedback loop maintains optimal chemokine concentrations for directional cell migration. Nat. Cell Biol. 22, 266–273. - PMC - PubMed
    1. Liu S.S., Liu C., Lv X.X.et al. (2021). The chemokine CCL1 triggers an AMFR‒SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis. Immunity 54, 2042–2056. - PubMed

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