机械转化
瘢痕疙瘩
串扰
免疫系统
发病机制
细胞生物学
焦点粘着
细胞内
肌动蛋白
癌症研究
医学
免疫学
生物
信号转导
病理
物理
光学
作者
Junxian Wen,Yingrou Tan,Yong Yao Chun,Timothy Thatt Yang Tan,Hong Liang Tey
摘要
Our comment on Min et al.’s study, “Novel therapeutic strategy for intractable keloids: Suppression of intracellular mechanotransduction and actin polymerisation via Rho-kinase pathway inhibition” highlights the importance of immune cell interactions with mechanical forces in keloid pathogenesis. While the authors effectively demonstrate the potential of inhibiting mechanotransduction in fibroblasts, we underscore the critical role of immune cells, particularly their response to ECM stiffness, in modulating fibrosis and suggest this crosstalk may reveal additional therapeutic targets.
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