ECM2026, 14-17 June 2026, Copenhagen, DenmarkIntro
Fibrosis research relies on models that can accurately reflect complex tissue architecture and human disease biology. In this session, we explore advances across ex vivo systems and animal models, highlighting how emerging platforms such as precision-cut tissue slices and whole-organ 3D imaging are improving translational relevance. Together, these approaches provide deeper insight into disease mechanisms and enable more predictive evaluation of anti-fibrotic therapies.
Get the full picture with quantitative 3D whole-organ imaging
Henrik H Hansen, Scientific Director, Gubra A/S
Abstract: Gubra is a disease-agnostic company specializing in peptide-based drug discovery and world-class preclinical contract research services.
Gubra is an industry leader in preclinical whole-organ imaging and AI-assisted histology. By leveraging tissue clearing and three-dimensional light sheet fluorescence microscopy (3D LSFM), we have established a high-throughput whole-organ imaging platform that enables automated, absolute quantification of clinically relevant histological endpoints at cellular resolution across all rodent organs and tissue samples from large animal models and humans. 3D LSFM imaging supports multiplex immunohistochemistry and in situ hybridization analyses, allowing comprehensive mapping of e.g. histopathological markers, tissue remodeling and drug distribution within intact organs. The platform has demonstrated broad utility across diverse preclinical disease models, including muscle atrophy, chronic kidney disease, diabetes, cardiovascular diseases, and CNS disorders.
This presentation introduces a pioneering whole-organ 3D imaging workflow for quantitative fibrosis assessment and highlights case studies. The platform enables micrometre-resolution visualization and volumetric quantification of collagen deposition across intact organs, addressing the sampling bias and limited spatial context inherent to conventional 2D histology. An AI-driven image analysis pipeline was developed to enable automated classification and quantification of fibrosis architecture and overall disease burden while preserving anatomical context.
Together, this automated 3D fibrosis analysis framework provides spatially resolved, organ-wide analysis suitable for high-throughput evaluation of anti-fibrotic drug efficacy.
Human Precision-Cut Tissue Slices as a Preclinical Platform for the Development & Testing of Novel Therapeutics
Lee Borthwick, FibroFind
Abstract: Precision Cut Tissue Slices (PCTS) from human organs provide a physiologically and structurally representative ex-vivo model that retains the native tissue architecture. Testing potential therapeutic targets and interrogating mechanisms underpinning disease pathophysiology in human PCTS allows us to assess their effectiveness and relevance to the clinical situation, overcoming many of the limitations of currently widely employed in-vivo rodent models and in-vitro 2D cell culture methodologies. FibroFind specialises in the application of advanced technologies for interrogating fibrosis biology. Leveraging our expertise, we have developed proprietary bioreactor-cultured PCTS that demonstrate exceptional performance in biomarker identification, toxicology, target discovery and drug efficacy evaluation. By harnessing robotics, AI-guided data analysis and a highly skilled team, FibroFind ensures unparalleled quality in all studies. Our portfolio includes PCTS from healthy and diseased lungs (IPF, ILD, COPD), kidneys and livers in 12, 24 and 96 well formats, allowing us to customise studies to meet your specific needs and deliver results that drive your research forward.
BigH3 in fibrosis and cancer
Nicholas Willumsen, Nordic Bioscience
Abstract: Fibroblast-driven deposition of extracellular matrix proteins, particularly type III collagen, is associated with poor clinical outcomes in liver fibrosis, fibrotic solid tumors such as pancreatic cancer, as well as other fibrotic diseases. PRO-C3 is a serum biomarker of active fibroblast-driven deposition type III collagen and has shown prognostic value in patients with liver fibrosis and pancreatic cancer, suggesting that pathways driving PRO-C3 elevation may represent therapeutic opportunities. In this study, we aimed to identify pathways associated with circulating PRO-C3 levels as potential targets for fibrotic diseases and cancer. A genome-wide association study (GWAS) in 4,968 subjects identified variants in TGFBI (BIGH3/βigH3) to be associated with elevated PRO-C3 levels. Additional analyses of serum samples from patients with pancreatic ductal adenocarcinoma and liver fibrosis confirmed significant correlations between PRO-C3 and BIGH3. Functional studies in fibroblasts, based on the well-established Scar-in-a-Jar model system, demonstrated that BIGH3 induced PRO-C3 production in a dose-dependent manner, which was inhibited by the anti-BIGH3 antibody 18B3, supporting a causal relationship. Inhibition of BIGH3 with 18B3 in a TGFβ-induced fibrosis model reduced PRO-C3 levels, indicating that BIGH3 contributes to pathological TGFβ signaling. Consistently, treatment with 18B3 also reduced the fibrotic activity of TGFβ-induced decellularized matrices. BIGH3 expression was detected in both macrophages and fibroblasts, particularly following TGFβ stimulation, supporting that BIGH3 acts as a downstream mediator of TGFβ-driven fibrosis. Together, these findings suggest that BIGH3 as a key mediator of TGFβ-induced fibrosis and support the therapeutic potential of targeting BIGH3 in patients with elevated PRO-C3 levels and fibrotic disease.
