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New insights into potential therapeutic approaches for COPD

News 2023-462 EN

Chronic obstructive pulmonary disease (COPD) is considered an incurable condition worldwide and one of the leading causes of death. Researchers from the DZL have now presented groundbreaking findings that offer a promising approach for the therapy of COPD.

The DZL researchers involved in this international study focused on Fibroblast Growth Factor (FGF)10, which is essential for lung morphogenesis in mice. Interestingly, polymorphisms in the human FGF10 gene correlate with an increased susceptibility to the development of COPD.

Analysis of FGF10 signaling pathways in human lung sections and isolated cells from healthy donors as well as smokers and patients with COPD revealed impaired FGF10 expression in the alveolar walls of COPD lungs and in primary interstitial fibroblasts. In contrast, increased FGF10 expression was observed in large lung vessels in COPD.

The research findings suggest that impaired FGF10 signaling in the alveolar walls is an integral part of the pathomechanism leading to the development of pulmonary emphysema and pulmonary hypertension (PH). Mice with disrupted FGF10 signaling pathways spontaneously developed lung emphysema, PH, and other typical pathomechanistic features usually attributed to cigarette smoke exposure.

In a promising therapeutic approach, overexpression of FGF10 in mice with established cigarette smoke- and elastase-induced lung emphysema and PH successfully restored alveolar and vascular structure. FGF10 treatment led to an initial increase in alveolar type 2 cells, which gradually returned to baseline levels as the FGF10-mediated repair process progressed.

Original publication:

Hadzic S, Wu CY, Gredic M, Pak O, Loku E, Kraut S, Kojonazarov B, Wilhelm J, Brosien M, Bednorz M, Seimetz M, Günther A, Kosanovic D, Sommer N, Warburton D, Li X, Grimminger F, Ghofrani HA, Schermuly RT, Seeger W, El Agha E, Bellusci S, Weissmann N. Fibroblast growth factor 10 reverses cigarette smoke- and elastase-induced emphysema and pulmonary hypertension in mice. Eur Respir J. 2023 Nov 9;62(5):2201606. doi: 10.1183/13993003.01606-2022. PMID: 37884305; PMCID: PMC10632559.

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