Fibrosis

Pulmonary disorders are among the most common medical conditions worldwide. Pulmonary fibrosis represents a severe and fast progressing lung disease, causing irreversible dysfunction of the organ. The disease is characterized by aberrant wound healing, excessive proliferation of fibroblasts, uncontrolled deposition of extracellular matrix, and destruction of the cellular architecture of the lung. So far, only two pharmacological treatments have been approved as anti-fibrotic drugs for clinical application (pirfenidone and nintedanib). However, both treatments can only slow down the progression of the disease and appear to cause serious side effects. In most cases, organ transplantation is the only option for patients. Hence, understanding the molecular mechanisms that are involved in the onset and progression of fibrotic response is an unmet medical need for the development of novel and more efficient treatments.

At Fraunhofer ITEM, a range of models to induce pulmonary fibrosis are established. This includes routinely employed and well-characterized in-vitro and in-vivo models to assess the pharmacological efficacy of new treatment options. In addition, a physiologically relevant ex-vivo model can be provided which enables investigation of important signaling pathways at different stages of the disease. The ability to conduct toxicological studies and clinical phase-I trials further complement the portfolio for translational fibrosis research at Fraunhofer ITEM.

Fibrosis

Bleomycin-induced pulmonary fibrosis in animals (IPF model)

Fibrosis in fresh human lung tissue