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A recent study by Xinzhi et al.1 in this issue of the BJD offers compelling new insights into the complex pathophysiology of dermatomyositis (DM). Leveraging the power of single-cell RNA sequencing (scRNAseq), they meticulously detailed a mechanistic framework, pinpointing distinct fibroblast populations, interferon-1 signalling and glycolytic pathways as central contributors to DM inflammation. Crucially, their work extends beyond mere description, demonstrating the therapeutic potential of blocking glycolytic pathways, which successfully alleviated symptoms in a mouse model of DM. This elegant study reinforces a growing body of literature that consistently highlights the indispensable role of scRNAseq in dissecting cellular heterogeneity. Indeed, recent reports2–4 have similarly leveraged scRNAseq to identify diverse fibroblast subtypes including secretory, mesenchymal and inflammatory populations, which are pivotal mediators of inflammation and itch across various skin conditions. Collectively, the studies underscore the critical capacity of scRNAseq to illuminate the intricate, often elusive, molecular and cellular pathways underpinning skin diseases, particularly those characterized by their therapeutic recalcitrance and poor understanding. The work by Xinzhi et al. stands as a testament to the ability of this technology to transform our understanding and guide future therapeutic strategies in challenging dermatological conditions such as DM.
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Oladipo et al. (2026) studied this question.
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