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Peer-reviewedCC BY 4.0Frontiers in Immunology

Mitochondria as immunometabolic hubs in psoriasis: pathogenic mechanisms and therapeutic prospects

  • Fangru Zhao1,2
  • Yaoxing Guo1,2
  • Xin Tong1,2
  • Xiangnan Zhou1,2
  • Yingdi Jiao1,2
  • Renjie Han1,2
  • Hongduo Chen1,2
  • Ruiqun Qi1,2
  1. 1Department of Dermatology, The Hospital of China Medical University
  2. 2Key Laboratory of Immunodermatology, Ministry of Education, and National Health Commission; National Joint Engineering Research Center for Theranostics of Immunological Skin Diseases
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Abstract

Psoriasis is a chronic, immune-mediated inflammatory dermatosis characterized by a profound dysregulation of immune-epithelial crosstalk. Beyond canonical ATP production, mitochondria function as essential intracellular immunometabolic hubs embedded within the cytokine-driven network of psoriatic lesions. Within this inflammatory niche, keratinocytes and immune cells undergo structural and metabolic adaptations. Aberrant mitochondrial stress byproducts—including mitochondrial reactive oxygen species (mtROS), oxidized mitochondrial DNA (mtDNA), and metabolic intermediates—act as secondary amplifiers that reinforce innate immune sensing and adaptive T cell responses, thereby sustaining a localized inflammatory loop. Here, we propose that targeting mitochondrial pathways provides a novel, stage-dependent therapeutic framework: stabilizing mitochondrial dynamics during acute flare-ups to halt inflammation, disrupting tissue-resident memory T (T RM ) cell metabolic fitness during the stable phase to avert relapse, and restoring regulatory T (Treg) cell oxidative phosphorylation (OXPHOS) during regression to re-establish peripheral immune tolerance. Transitioning from broad immunosuppression to precision mitochondrial modulation offers a promising paradigm for cell-specific psoriasis interventions.

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Cite

BibTeXRIS
BibTeX
@article{zhao2026mitochondria,
  title = {{Mitochondria as immunometabolic hubs in psoriasis: pathogenic mechanisms and therapeutic prospects}},
  author = {Fangru Zhao and Yaoxing Guo and Xin Tong and Xiangnan Zhou and Yingdi Jiao and Renjie Han and Hongduo Chen and Ruiqun Qi},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1991331},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991331/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Mitochondria as immunometabolic hubs in psoriasis: pathogenic mechanisms and therapeutic prospects
AU  - Fangru Zhao
AU  - Yaoxing Guo
AU  - Xin Tong
AU  - Xiangnan Zhou
AU  - Yingdi Jiao
AU  - Renjie Han
AU  - Hongduo Chen
AU  - Ruiqun Qi
PY  - 2026
DA  - 2026/10/23
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1991331
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1991331/full
AB  - Psoriasis is a chronic, immune-mediated inflammatory dermatosis characterized by a profound dysregulation of immune-epithelial crosstalk. Beyond canonical ATP production, mitochondria function as essential intracellular immunometabolic hubs embedded within the cytokine-driven network of psoriatic lesions. Within this inflammatory niche, keratinocytes and immune cells undergo structural and metabolic adaptations. Aberrant mitochondrial stress byproducts—including mitochondrial reactive oxygen species (mtROS), oxidized mitochondrial DNA (mtDNA), and metabolic intermediates—act as secondary amplifiers that reinforce innate immune sensing and adaptive T cell responses, thereby sustaining a localized inflammatory loop. Here, we propose that targeting mitochondrial pathways provides a novel, stage-dependent therapeutic framework: stabilizing mitochondrial dynamics during acute flare-ups to halt inflammation, disrupting tissue-resident memory T (T RM ) cell metabolic fitness during the stable phase to avert relapse, and restoring regulatory T (Treg) cell oxidative phosphorylation (OXPHOS) during regression to re-establish peripheral immune tolerance. Transitioning from broad immunosuppression to precision mitochondrial modulation offers a promising paradigm for cell-specific psoriasis interventions.
SN  - 1664-3224
ER  -