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This study identified three hub genes—BMP4, POSTN, and WNT5A—that are closely associated with keloid fibroblast hyperplasia, suggesting they may serve as potential biomarkers for inhibiting this condition. Further research is necessary to fully understand their roles in keloid development.

Keloid fibroblasts cause itch and pain by releasing more histamine.

In this study, researchers conducted single-cell RNA sequencing to reveal that proinflammatory fibroblasts and vascular endothelial cells play significant roles in the immune microenvironment of keloids, suggesting potential targets for new therapeutic approaches.

This study found that a key gene signature, including FGF11, highlights the immunologic nature of keloid lesions, distinguishing them from normal fibroblasts and scars.

In this study, researchers identified that keloid fibroblasts respond to neurotransmitters from catecholaminergic nerves by producing bone matrix proteins, mediated by β1-adrenergic receptor activation, leading to fibro-osseous reprogramming; blocking this signaling in a rodent model prevented the development of keloid-like pathology.