ArticleEuropean respiratory review : an official journal of the European Respiratory Society2026
Selective phosphodiesterase 4B inhibition in fibrotic lung disease: a scoping review of vascular-immune mechanisms and extrapulmonary implications.
Article in European respiratory review : an official journal of the European Respiratory Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPreferential phosphodiesterase 4B (PDE4B) inhibition with nerandomilast has demonstrated attenuation of forced vital capacity decline in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis. Because PDE4 enzymes regulate cAMP-dependent inflammatory and endothelial signalling, class-level PDE4 inhibition has been consistently linked to vascular-immune pathways. Whether preferential PDE4B inhibition reproduces these effects remains uncertain.
objectivesTo map the available mechanistic and translational literature on extrapulmonary or systemic biological effects of PDE4/PDE4B inhibition and to place nerandomilast trial findings within that framework without inferring clinical efficacy outside pre-specified trial outcomes.
methodsWe performed a the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews informed scoping review of PubMed/MEDLINE from database inception to 1 March 2026. Eligible studies included pre-clinical, translational and clinical reports addressing endothelial, immune, microvascular or organ-level effects of PDE4/PDE4B modulation. Evidence was charted and narratively synthesised rather than quantitatively pooled.
results71 studies were included. Experimental data (primarily derived from class-level PDE4 inhibition) consistently link these pathways to modulation of endothelial permeability, leukocyte-endothelial adhesion, thromboinflammatory signalling, and macrophage resolution programmes across pulmonary and extrapulmonary models. However, most extrapulmonary evidence derives from class-level PDE4 biology rather than nerandomilast-specific investigations, and clinical evidence for extrapulmonary benefit in fibrotic lung disease remains indirect.
conclusionsBecause PDE4 enzymes regulate cAMP-dependent inflammatory and endothelial signalling, class-level PDE4 inhibition has been consistently linked to modulation of vascular-immune pathways. Whether preferential PDE4B inhibition reproduces these effects in humans remains to be established. While at present, extrapulmonary clinical benefit in fibrotic lung disease remains unproven, future studies should prospectively evaluate systemic biomarkers and organ-level outcomes rather than relying on
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