ArticleiScience2026
Single-cell transcriptomics reveals that tenocyte-derived MIF contributes to tendon injury pathogenesis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Tendon injury is accompanied by inflammation and pathological tissue remodeling, yet the underlying cellular and molecular mechanisms remain incompletely understood. Reanalysis of single-cell transcriptomic data across tendon-healing time points revealed dynamic cellular heterogeneity, including eight transcriptionally distinct mesenchymal subpopulations and eight immune-cell clusters. CellChat predicted relatively strong outgoing signaling from mesenchymal populations and incoming signaling to myeloid populations during repair. MIF-associated communication between selected tenocyte and myeloid populations was predicted to increase during the acute injury stage, involving the MIF-(CD74+CXCR4) and MIF-ACKR3 ligand-receptor pairs. MIF expression increased in injured tendon and was associated with inflammatory, apoptotic, stress-related, and histopathological changes. Pharmacological treatment with 4-IPP delivered in a photocrosslinked F127DA hydrogel formulation (F127@4-IPP) attenuated inflammation and osteogenic changes and improved histological outcomes in the mouse injury model. These findings support further evaluation of MIF-associated signaling and F127@4-IPP intervention in tendon injury.
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