Beta‐catenin non‐canonical pathway: A potential target for inflammatory and hyperproliferative state via expression of transglutaminase 2 in psoriatic skin keratinocyte

Gaurav Gupta, Yogendra Singh, Juhi Tiwari, Abhay Raizaday, Khalid Saad Alharbi, Fahad A. Al‐abbasi, Imran Kazmi, Saurabh Satija, Murtaza M. Tambuwala, Hari Prasad Devkota, Anand Krishnan, Dinesh Kumar Chellappan, Kamal Dua

Research output: Contribution to journalReview article

Abstract

Psoriasis is a chronic, local as well as a systemic, inflammatory skin condition. Psoriasis influences the quality of life up to 3.8% of the population and occurs often between 15 and 30 years of age. Specific causes are linked to psoriasis, including the interleukin IL-23 / IL-17 Axis, human antigen leucocyte (HLA), and tumor necrosis factor-α (TNF-α). Secukinumab is a monoclonal antibody that specifically binds and neutralizes IL-17A required in the treatment of Psoriasis. The signaling pathways of Wnt govern multiple functions of cell-like fate specification, proliferation, polarity, migration, differentiation with their signaling controlled rigorously, given that dysregulation caused by various stimuli, can lead to alterations in cell proliferation, apoptosis, and human inflammatory disease. Current data has supported non-canonical Wnt signaling pathways in psoriasis development, particularly Wnt5a activated signaling cascades. These interconnected factors are significant in interactions between immune cells, keratinocytes, and inflammatory factors due to a higher degree of transglutaminase 2, mediated by activation of the keratinocyte hyperproliferation of the psoriatic patient's epidermis. This study discusses the pathology of Wnt5a signaling and its involvement in the epidermal inflammatory effects of psoriasis with other related pathways.
Original languageEnglish
Article numbere14209
Number of pages11
JournalDermatologic Therapy
Early online date20 Aug 2020
DOIs
Publication statusE-pub ahead of print - 20 Aug 2020

Keywords

  • WNT5A
  • Wnt/β-catenin signaling
  • chemokines
  • cytokines
  • dendritic cells
  • inflammation
  • non-canonical Wnt signaling
  • nuclear factor-kappa B
  • transglutaminase 2
  • tumor necrosis factor-α

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