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αv integrins: key regulators of tissue fibrosis

Kylie P Conroy1, Laura J Kitto1, Neil C Henderson2

  • 1MRC Centre for Inflammation Research, The Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.

Cell and Tissue Research
|May 4, 2016
PubMed

Insights

Targeting alpha-v (αv) integrins shows promise for treating fibrotic diseases. These cell adhesion molecules are key regulators of tissue repair and fibrosis, making them a potential therapeutic target.

Area of Science:

  • Cell Biology
  • Molecular Medicine
  • Pathology

Background:

  • Chronic tissue injury leads to fibrosis, disrupting organ architecture and function, necessitating novel anti-fibrotic therapies.
  • Fibrogenesis involves complex interactions between cellular and extracellular matrix components during wound healing.
  • Integrins, transmembrane cell adhesion molecules, are crucial mediators of cell-matrix and intercellular communications.

Purpose of the Study:

  • To review the current understanding of alpha-v (αv) integrin-mediated regulation of fibrogenesis.
  • To explore the therapeutic potential of targeting specific αv integrins for treating fibrotic diseases.

Main Methods:

  • Literature review focusing on the role of integrins in fibrosis.
  • Analysis of mechanisms by which αv integrins regulate fibrogenesis.
  • Examination of studies investigating the modulation of αv integrins in various fibrotic conditions.

Main Results:

  • Integrins are central to the communication network regulating tissue fibrosis.
  • Modulation of αv integrin family members has demonstrated significant effects on fibrosis across multiple organs.
  • Specific αv integrins are intimately involved in the initiation, maintenance, and resolution of tissue fibrosis.

Conclusions:

  • Targeting specific αv integrins represents a promising therapeutic strategy for a wide range of fibrotic diseases.
  • Understanding αv-integrin-mediated fibrogenesis mechanisms can guide the development of effective anti-fibrotic treatments.
Keywords:
Extracellular matrixFibrosisIntegrinsMyofibroblastsTGFβ

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