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Rejuvenating old lungs: Ain’t no tonic like a drop of retinoic
  1. Reinoud Gosens1,2,
  2. John-Poul Ng-Blichfeldt3
  1. 1 Molecular Pharmacology, University of Groningen, Groningen, The Netherlands
  2. 2 Groningen Research Institute for Asthma and COPD, University of Groningen, Groningen, The Netherlands
  3. 3 MRC Laboratory of Molecular Biology, Cambridge, UK
  1. Correspondence to Dr Reinoud Gosens, Molecular Pharmacology, University of Groningen, Groningen, The Netherlands; r.gosens{at}rug.nl

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One of the main challenges of experimental respiratory medicine today is the development of therapies that could support lung regeneration, leading to restoration of lung structure and function, in chronic lung diseases such as idiopathic pulmonary fibrosis (IPF). Current therapies such as pirfenidone and nintedanib slow down progression of the disease, but are insufficient to modify the underlying disease process to the extent that progression can be halted or that lung regeneration can be achieved.1 Accordingly, new regenerative therapies will need to be developed guided by insights into the mechanistic underpinnings of defective alveolar regeneration. This challenge is on, not just for IPF, but also for other chronic diseases such as chronic obstructive pulmonary disease (COPD), and is complicated by the limited endogenous regenerative capacity of the ageing lung as the background against which these diseases often develop.

Retinoids are among the most widely studied classes of drugs with putative proregenerative capacity. Retinoic acid signals by binding to nuclear retinoic acid receptors which form heterodimeric complexes with retinoid X receptors to effect gene expression in a variety of cells. Both retinoic acid derivatives and retinoid X receptor ligands have been studied for their proregenerative effects, mostly in experimental models of COPD, and were found to enhance alveolar regeneration in the emphysematous lung.2 …

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Footnotes

  • Contributors RG and J-PN-B drafted the manuscript and approved the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests RG has received research funding, through the institution, from Aquilo BV, from Boehringer Ingelheim, from Chiesi, and from Sanofi-Aventis.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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