Scholarlink

Background <p>The differentiation of skin dermal fibroblast into myofibroblast is a critical process in tissue repair and granulation tissue formation, directly affecting the progression of wound healing. While autophagy has been implicated in regulating dermal fibroblast differentiation during wound repair, the underlying molecular mechanisms remain incompletely defined.</p> Methods and results <p>In the current study, Transforming Growth Factor-Beta 1 (TGFβ1) was applied to induce the differentiation of skin dermal fibroblast into myofibroblast. We demonstrated that the activation of autophagy by TGFβ1 stimulation and p38 Mitogen-Activated Protein Kinase (p38/MAPK) coincided with an increase in stathmin expression. Moreover, the inhibition of p38/MAPK, transfection of small interfering RNA of stathmin or beclin1 significantly suppressed autophagy and differentiation of skin dermal fibroblast into myofibroblast. In contrast, p38/MAPK activation or stathmin overexpression, led to autophagy induction and fibroblast differentiation under TGFβ1 stimulation.</p> Conclusions <p>Our findings elucidate a novel role of stathmin in regulating differentiation of skin dermal fibroblast into myofibroblast, and suggest its potential as a therapeutic target for clinical wound healing interventions.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Stathmin-mediated autophagy drives the differentiation of dermal fibroblast into myofibroblast under TGFβ1 stimulation

  • 期刊论文

  • 发表日期：

    2025年12月6日

查看全文
  • Hui Tang,
  • Luqi Yang,
  • Yanhai Feng,
  • Jianxin Wu,
  • Yi Liang,
  • Zhenglin Li,
  • Lingbo Li,
  • Wan Zhao,
  • Xiaolin Deng,
  • Dan Luo,
  • Xia Lei,
  • Lingfei Li

摘要

Background

The differentiation of skin dermal fibroblast into myofibroblast is a critical process in tissue repair and granulation tissue formation, directly affecting the progression of wound healing. While autophagy has been implicated in regulating dermal fibroblast differentiation during wound repair, the underlying molecular mechanisms remain incompletely defined.

Methods and results

In the current study, Transforming Growth Factor-Beta 1 (TGFβ1) was applied to induce the differentiation of skin dermal fibroblast into myofibroblast. We demonstrated that the activation of autophagy by TGFβ1 stimulation and p38 Mitogen-Activated Protein Kinase (p38/MAPK) coincided with an increase in stathmin expression. Moreover, the inhibition of p38/MAPK, transfection of small interfering RNA of stathmin or beclin1 significantly suppressed autophagy and differentiation of skin dermal fibroblast into myofibroblast. In contrast, p38/MAPK activation or stathmin overexpression, led to autophagy induction and fibroblast differentiation under TGFβ1 stimulation.

Conclusions

Our findings elucidate a novel role of stathmin in regulating differentiation of skin dermal fibroblast into myofibroblast, and suggest its potential as a therapeutic target for clinical wound healing interventions.