This letter evaluates collagen I–DDR1 signaling in keloid inflammation, highlighting implications for dual-target therapy.
This letter critically evaluates the recent study by Hu et al. on collagen I–DDR1 signaling in keloid inflammation, highlighting its role in activating NF-κB and STAT3 pathways. We discuss the potential of dual-target therapy involving DDR1 and ARF6 inhibition and identify areas for further exploration, including the involvement of co-receptors, intermediate signaling pathways, and collagen remodeling. These insights may guide future therapeutic strategies for keloid treatment.
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Wang et al. (2026) studied this question.
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