Pathological insight into 5-ht2b receptor activation in fibrosing interstitial lung diseases

Anna Löfdahl, Göran Tornling, Jenny Wigén, Anna Karin Larsson-Callerfelt, Christina Wenglén, Gunilla Westergren-Thorsson

Research output: Contribution to journalReview articlepeer-review

Abstract

Interstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 con-ditions, of which primarily idiopathic pulmonary fibrosis (IPF), idiopathic nonspecific interstitial pneumonia, hypersensitivity pneumonitis, ILD associated with autoimmune diseases and sarcoidosis may present a progressive fibrosing (PF) phenotype. Despite different aetiology and histopathological patterns, the PF-ILDs have similarities regarding disease mechanisms with self-sustaining fibrosis, which suggests that the diseases may share common pathogenetic pathways. Previous studies show an enhanced activation of serotonergic signaling in pulmonary fibrosis, and the serotonin (5-HT)2 receptors have been implicated to have important roles in observed profibrotic actions. Our research findings in support by others, demonstrate antifibrotic effects with 5-HT2B receptor antagonists, alleviating several key events common for the fibrotic diseases such as myofibroblast differentiation and connective tissue deposition. In this review, we will address the potential role of 5-HT and in particular the 5-HT2B receptors in three PF-ILDs: ILD associated with systemic sclerosis (SSc-ILD), ILD associated with rheumatoid arthritis (RA-ILD) and IPF. Highlighting the converging pathways in these diseases discloses the 5-HT2B receptor as a potential disease target for PF-ILDs, which today have an urgent unmet need for therapeutic strategies.

Original languageEnglish
Article number225
Number of pages19
JournalInternational Journal of Molecular Sciences
Volume22
Issue number1
DOIs
Publication statusPublished - 2021

Subject classification (UKÄ)

  • Respiratory Medicine and Allergy
  • Cell and Molecular Biology

Keywords

  • 5-HT
  • 5-HT receptor antagonism
  • Fibrosis
  • ILD

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