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<p>Psoriasis is an immune-mediated chronic inflammatory skin disease, with over 100&#xa0;million people affected worldwide. This disease is accompanied by significant lipid metabolism disorders, affecting the circulatory system and skin tissue. This study found that patients with psoriasis have abnormal lipid metabolism, among which the levels of long-chain fatty acids (LCFAs) and mitochondrial pyruvate carriers (MPC) in mesenchymal stem cells (MSCs) are significantly lower than those in healthy controls. It is worth noting that the key regulatory factor of lipid metabolism, ADIPOQ (adiponectin), is down-regulated in psoriasis and functions dependent on LCFAs oxidation and carnitine palmitoyltransferase 1 (CPT1) under conditions of high substrate demand. Mechanically, ADIPOQ significantly inhibits the proliferation of normal human keratinocytes (NHEKs) by activating the p-AMPK/AMPK (AMP-activated protein kinase) signal and enhancing the activity of CPT1 enzyme. In the imQ-induced psoriasis-like mouse model, exogenous ADIPOQ intervention can improve epidermal thickening and down-regulate the expression of inflammatory factors through the AMPK-CPT1 pathway. In conclusion, this study reveals that ADIPOQ treatment can inhibit the proliferation of NHEKs by reshaping lipid metabolism, thereby delaying the progression of psoriasis. Targeting this metabolic pathway may provide a new strategy for clinical intervention.</p>

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ADIPOQ regulates lipid metabolism by activating AMPK/CPT-1 pathway to attenuate the proliferation of psoriasis lesions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Jianxiao Xing,
  • Jiao Li,
  • Aihong Peng,
  • Ying Wang,
  • Yuanjun Yao,
  • Yali He,
  • Junqin Li,
  • Kaiming Zhang

摘要

Psoriasis is an immune-mediated chronic inflammatory skin disease, with over 100 million people affected worldwide. This disease is accompanied by significant lipid metabolism disorders, affecting the circulatory system and skin tissue. This study found that patients with psoriasis have abnormal lipid metabolism, among which the levels of long-chain fatty acids (LCFAs) and mitochondrial pyruvate carriers (MPC) in mesenchymal stem cells (MSCs) are significantly lower than those in healthy controls. It is worth noting that the key regulatory factor of lipid metabolism, ADIPOQ (adiponectin), is down-regulated in psoriasis and functions dependent on LCFAs oxidation and carnitine palmitoyltransferase 1 (CPT1) under conditions of high substrate demand. Mechanically, ADIPOQ significantly inhibits the proliferation of normal human keratinocytes (NHEKs) by activating the p-AMPK/AMPK (AMP-activated protein kinase) signal and enhancing the activity of CPT1 enzyme. In the imQ-induced psoriasis-like mouse model, exogenous ADIPOQ intervention can improve epidermal thickening and down-regulate the expression of inflammatory factors through the AMPK-CPT1 pathway. In conclusion, this study reveals that ADIPOQ treatment can inhibit the proliferation of NHEKs by reshaping lipid metabolism, thereby delaying the progression of psoriasis. Targeting this metabolic pathway may provide a new strategy for clinical intervention.