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Current evidence suggests that cyclic adenosine monophosphate (cAMP) mitigates lung fibroblast proliferation\n                      <jats:italic>via<\/jats:italic>\n                      the protein kinase A pathway, but the impact of exchange proteins directly activated by cAMP 1 (Epac1) on IPF remains unexplored.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To investigate the role of Epac1 in IPF progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We examined lung samples from IPF patients and controls, and from a bleomycin-induced mouse model of pulmonary fibrosis. The effects of Epac were analysed in knockout mice and through modulation using viral vectors. The Epac1-specific small compound inhibitor AM-001 was evaluated\n                      <jats:italic>in vitro<\/jats:italic>\n                      using lung fibroblasts from patients with IPF,\n                      <jats:italic>in vivo<\/jats:italic>\n                      in bleomycin mice and\n                      <jats:italic>ex vivo<\/jats:italic>\n                      in IPF precision-cut lung slices.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Increased Epac1 expression was observed in lung tissues from IPF patients, fibrotic fibroblasts and bleomycin-challenged mice. Genetic or pharmacological inhibition of Epac1 with AM-001 decreased proliferation in normal and IPF fibroblasts, and reduced expression of profibrotic markers such as \u03b1-smooth muscle actin, transforming growth factor-\u03b2\/SMAD family member 2\/3, and interleukin-6\/signal transducer and activator of transcription 3 pathways. Epac1-specific inhibition consistently protected against bleomycin-induced lung injury and fibrosis, suggesting significant therapeutic potential. Global gene expression profiling indicated a reduced profibrotic gene signature and neddylation pathway components in Epac1-deficient fibroblasts and human-derived lung cells. Mechanistically, the protective effects may involve inhibiting the neddylation pathway and preventing neural precursor cell expressed, developmentally downregulated 8 (NEDD8) activation, which in turn reduces the degradation of forkhead box protein O3 by NEDD8. Additionally, these effects may be enhanced while also limiting the proliferation of lung-infiltrating monocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings demonstrate that Epac1 regulates fibroblast activity in pulmonary fibrosis, and that targeting Epac1 with the pharmacological specific inhibitor AM-001 offers a promising therapeutic approach for treating IPF disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1183\/13993003.02250-2024","type":"journal-article","created":{"date-parts":[[2025,7,10]],"date-time":"2025-07-10T14:40:15Z","timestamp":1752158415000},"page":"2402250","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Pharmacological inhibition of Epac1 protects against pulmonary fibrosis by blocking FoxO3a 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