Keloid is a fibrotic dermal disease characterized by an abnormal increase in fibroblast proliferation and invasion. These pathological behaviours may be related to the heterogeneity of keloid fibroblasts (KFs); however, because of a lack of effective biomarkers for KFs it is difficult to study the underlying mechanism. Our previous studies revealed that the expansion of CD26⁺ KFs was responsible for increased keloid proliferation and invasion capabilities; the intrinsic relationship and mechanism between CD26 and keloid is therefore worthy of further investigation. The aim of this study was to explore molecular mechanisms in the process of CD26 upregulated KFs proliferation and invasion abilities, and provide more evidence for CD26 as an effective biomarker of keloid and a new clinical therapeutic target.

中文翻译：

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CD26 通过 IGF-1 诱导的 PI3K/AKT/mTOR 通路上调瘢痕疙瘩成纤维细胞的增殖和侵袭

瘢痕疙瘩是一种纤维化皮肤疾病，其特征是成纤维细胞增殖和侵袭异常增加。这些病理行为可能与瘢痕疙瘩成纤维细胞（KFs）的异质性有关；然而，由于缺乏有效的 KF 生物标志物，很难研究其潜在机制。我们之前的研究表明，CD26 ⁺ KFs 的扩增是增加瘢痕疙瘩增殖和侵袭能力的原因；因此CD26与瘢痕疙瘩的内在关系和机制值得进一步研究。本研究旨在探索CD26上调KFs增殖和侵袭能力过程中的分子机制，为CD26作为瘢痕疙瘩的有效生物标志物和新的临床治疗靶点提供更多证据。