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Updated: Feb 20, 2026

Author Spotlight: Advancing Real-Time cAMP Detection in Cells Using cADDis Biosensor
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Author Spotlight: Advancing Real-Time cAMP Detection in Cells Using cADDis Biosensor

Published on: March 22, 2024

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Mechanistic basis for the antifibrotic actions of cAMP-based therapies

Marc Peters-Golden1,2, Sean M Fortier3,2

  • 1Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA petersm@umich.edu.

European Respiratory Review : an Official Journal of the European Respiratory Society
|February 18, 2026
PubMed

Insights

New antifibrotic therapies for idiopathic pulmonary fibrosis target the cAMP pathway. Understanding how cAMP elevation combats lung fibrosis offers new treatment strategies.

Area of Science:

  • Pulmonary Medicine
  • Pharmacology
  • Cell Biology

Background:

  • Idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases (ILDs) have a significant human and economic impact.
  • Current therapies for ILDs offer limited utility, highlighting the need for novel treatment approaches.
  • Two new antifibrotic agents, nerandomilast and treprostinil, which increase intracellular cyclic adenosine monophosphate (cAMP), are emerging.

Purpose of the Study:

  • To elucidate the mechanistic basis for the therapeutic potential of cAMP elevation in fibrotic lung diseases.
  • To review the pathogenesis of lung fibrosis, the cAMP signaling pathway, and its dysregulation in disease.
  • To explore the multifaceted actions of cAMP in counteracting the cellular abnormalities driving fibrotic lung diseases.

Main Methods:

  • Review of existing literature on the pathogenesis of fibrotic lung disease.
  • Analysis of the cAMP signaling pathway's structure and function.
  • Examination of how cAMP elevation impacts immune cells, fibroblasts, and epithelial cells in fibrotic contexts.

Main Results:

  • cAMP signaling is disrupted in fibrotic lung diseases.
  • Elevated cAMP levels demonstrate pleiotropic antifibrotic effects by modulating immune, fibroblast, and epithelial cell functions.
  • The antifibrotic potential of cAMP elevation is currently underappreciated in clinical and research settings.

Conclusions:

  • Targeting the cAMP pathway presents a promising therapeutic strategy for managing fibrotic lung diseases.
  • Further research is needed to optimize interventions that leverage cAMP signaling for treating lung fibrosis.
  • Understanding the detailed mechanisms of cAMP's antifibrotic actions can guide the development of more effective therapies.

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