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<p>Psoriasis is an inflammatory skin disease marked by excessive proliferation of keratinocytes, and there is accumulating evidence indicating its association with Parkinson’s disease (PD). However, the molecular link between these two diseases remains elusive. Herein, we identify a potential role for parkin, a PD-related E3 ubiquitin ligase, in the inhibition of psoriasis pathogenesis. The level of parkin is reduced in psoriatic skin both in clinical samples and in mouse models. Parkin-deficient mice exhibit epidermal hyperplasia, increased keratinocyte proliferation, and enhanced susceptibility to psoriasis. Mechanistically, parkin interacts with γ-tubulin, a centrosomal protein required for microtubule organization, and mediates γ-tubulin ubiquitination and proteasomal degradation. Reduction of parkin in psoriatic skin leads to abnormal accumulation of γ-tubulin and disrupts the proper organization of microtubules in the epidermis, resulting in the hyperproliferation of keratinocytes. These findings reveal a previously unrecognized role for parkin in epidermal physiology and pathology, and offer novel insights into the crosstalk between psoriasis and PD.</p>

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The parkin-γ-tubulin axis regulates epidermal homeostasis and is associated with the susceptibility to psoriasis

  • 期刊论文

  • 发表日期：

    2026年2月27日

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  • Yuanyuan Liu,
  • Shaoze Yan,
  • Jiaxuan Wang,
  • Dan Dong,
  • Shaodong Yan,
  • Hanxiao Yin,
  • Kai Liu,
  • Min Liu,
  • Hong Liu,
  • Dengwen Li,
  • Jinmin Gao,
  • Wei Xie,
  • Jun Zhou

摘要

Psoriasis is an inflammatory skin disease marked by excessive proliferation of keratinocytes, and there is accumulating evidence indicating its association with Parkinson’s disease (PD). However, the molecular link between these two diseases remains elusive. Herein, we identify a potential role for parkin, a PD-related E3 ubiquitin ligase, in the inhibition of psoriasis pathogenesis. The level of parkin is reduced in psoriatic skin both in clinical samples and in mouse models. Parkin-deficient mice exhibit epidermal hyperplasia, increased keratinocyte proliferation, and enhanced susceptibility to psoriasis. Mechanistically, parkin interacts with γ-tubulin, a centrosomal protein required for microtubule organization, and mediates γ-tubulin ubiquitination and proteasomal degradation. Reduction of parkin in psoriatic skin leads to abnormal accumulation of γ-tubulin and disrupts the proper organization of microtubules in the epidermis, resulting in the hyperproliferation of keratinocytes. These findings reveal a previously unrecognized role for parkin in epidermal physiology and pathology, and offer novel insights into the crosstalk between psoriasis and PD.