Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling

Wenlu Jiang, Xiaoxiao Pang, Pin Ha, Chenshuang Li, Grace Xinlian Chang, Yuxin Zhang, Lawrence A. Bossong, Kang Ting (), Chia Soo () and Zhong Zheng ()
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Wenlu Jiang: Los Angeles
Xiaoxiao Pang: Stomatological Hospital of Chongqing Medical University
Pin Ha: Los Angeles
Chenshuang Li: University of Pennsylvania
Grace Xinlian Chang: Los Angeles
Yuxin Zhang: Stomatological Hospital of Chongqing Medical University
Lawrence A. Bossong: Princeton University
Kang Ting: American Dental Association Forsyth Institute
Chia Soo: Los Angeles
Zhong Zheng: Los Angeles

Nature Communications, 2025, vol. 16, issue 1, 1-20

Abstract: Abstract Activated myofibroblasts deposit extracellular matrix material to facilitate rapid wound closure that can heal scarlessly during fetal development. However, adult myofibroblasts exhibit a relatively long life and persistent function, resulting in scarring. Thus, understanding how fetal and adult tissue regeneration differs may serve to identify factors that promote more optimal wound healing in adults with little or less scarring. We previously found that matricellular proteoglycan fibromodulin is one such factor promoting more optimal repair, but the underlying molecular and cellular mechanisms for these effects have not been fully elucidated. Here, we find that fibromodulin induces myofibroblast apoptosis after wound closure to reduce scarring in small and large animal models. Mechanistically, fibromodulin accelerates and prolongs the formation of the interleukin 1β-interleukin 1 receptor type 1-interleukin 1 receptor accessory protein ternary complex to increase the apoptosis of myofibroblasts and keloid- and hypertrophic scar-derived cells. As the persistence of myofibroblasts during tissue regeneration is a key cause of fibrosis in most organs, fibromodulin represents a promising, broad-spectrum anti-fibrotic therapeutic.

Date: 2025
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DOI: 10.1038/s41467-025-58906-z

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