Scientific article
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The Role of Hippo Signaling Pathway and ILK in the Pathophysiology of Human Hypertrophic Scars and Keloids: An Immunohistochemical Investigation

Published inCells, vol. 11, no. 21, 3426
Publication date2022-10-29
First online date2022-10-29
Abstract

Background: Keloids and hypertrophic scars are characterized by abnormal fibroblast activation and proliferation. While their molecular pathogenesis remains unclear, myofibroblasts have been associated with their development. Hippo pathway effectors YAP/TAZ promote cell proliferation and matrix stiffening. Integrin-linked kinase (ILK), a central component of focal adhesions that mediates cell-matrix interactions, has been linked to tissue repair and fibrosis. The aim of this study was to investigate the expression of key Hippo pathway molecules and ILK in hypertrophic scars and keloids.

Methods: YAP/TAZ, TEAD4, ILK and a-SMA expression were evaluated by immunohistochemistry in keloids (n = 55), hypertrophic scars (n = 38) and normal skin (n = 14).

Results: The expression of YAP/TAZ, TEAD4, ILK and a-SMA was higher in fibroblasts of keloids compared to hypertrophic scars while negative in normal skin. There was a significant positive correlation between the expression of ILK and Hippo pathway effectors.

Conclusions: Our results suggest that the deregulation of Hippo signaling and ILK are implicated in keloid and hypertrophic scar formation.

Keywords
  • Hippo pathway
  • ILK
  • Hypertrophic scars
  • Keloids
  • Scars
  • Wound healing
  • Humans
  • Cicatrix, Hypertrophic / metabolism
  • Cicatrix, Hypertrophic / pathology
  • Keloid / metabolism
  • Hippo Signaling Pathway
  • Wound Healing
  • DNA-Binding Proteins / metabolism
  • Muscle Proteins / metabolism
  • Transcription Factors
Citation (ISO format)
PETROU, Ilias et al. The Role of Hippo Signaling Pathway and ILK in the Pathophysiology of Human Hypertrophic Scars and Keloids: An Immunohistochemical Investigation. In: Cells, 2022, vol. 11, n° 21, p. 3426. doi: 10.3390/cells11213426
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Identifiers
Additional URL for this publicationhttps://www.mdpi.com/2073-4409/11/21/3426
Journal ISSN2073-4409
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Creation21/11/2022 13:41:00
First validation21/11/2022 13:41:00
Update16/03/2023 10:30:20
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