ECM Remodeling and Precision Trials in Pulmonary Diseases | Webinar

From Heterogeneity to Biology: ECM Remodeling and Precision Trials in Pulmonary Diseases

Overview

Watch this webinar to explore whether current approaches truly capture the underlying biology of pulmonary diseases such as COPD and lung cancer. This session focuses on extracellular matrix (ECM) remodeling as a central disease mechanism, its role in disease heterogeneity, and how ECM-derived biomarkers may support precision trials and improved prognostic assessment.

Agenda

  • Welcome and introduction
  • COPD heterogeneity and extracellular matrix remodeling as a core disease mechanism
  • ECM biomarkers as tools for disease activity and prognosis – Assessing critical pathways of disease
  • From COPD to Lung Cancer – The ECM as a pro-tumor environment

Scientific topics

Chronic obstructive pulmonary disease is traditionally defined and monitored using functional parameters such as airflow limitation. However, COPD is biologically heterogeneous, reflecting distinct pathological processes that are not fully captured by spirometry alone. Structural remodeling of the extracellular matrix (ECM) is increasingly recognized as a central mechanism underlying disease progression.

Persistent inflammation, protease–antiprotease imbalance, and dysregulated tissue repair drive continuous ECM turnover in the lungs. This remodeling alters airway structure, contributes to emphysematous destruction, and shapes the microenvironment that sustains chronic disease activity. Understanding these matrix-driven processes provides a biologically grounded framework for redefining disease subtypes.

ECM-derived biomarkers offer the potential to quantify ongoing tissue remodeling in real time. By reflecting specific collagen formation and degradation pathways, these biomarkers may enable improved assessment of disease activity, stratification of patients, and evaluation of therapeutic response in precision clinical trials.

Beyond COPD progression, ECM remodeling also influences the broader pulmonary microenvironment. Altered matrix composition and stiffness can create conditions that support tumor initiation and growth, linking chronic lung disease biology to lung cancer risk. Exploring the ECM as a pro-tumor niche expands the discussion from chronic inflammation to oncogenic transformation.

This webinar examines how shifting focus from symptoms and physiology to measurable biology may redefine endpoints, improve patient selection in trials, and advance precision medicine in COPD.

Speakers

Dr. Janette Burgess

  • Dr. Janette Burgess is Professor of Extracellular Matrix in Disease Pathogenesis at the University Medical Center Groningen and a Rosalind Franklin Fellow.
  • Her research focuses on the role of the extracellular matrix (ECM) in lung diseases, particularly how structural changes in lung tissue and airways drive disease development and progression.
  • She investigates whether ECM alterations are causal drivers or consequences of pathology in chronic lung conditions.
  • Dr. Burgess leads translational research integrating primary human lung cells, patient tissue samples, and clinical data to characterize ECM remodeling.
  • Her group employs advanced in vitro models, ex vivo human lung tissue systems, and high-resolution microscopy to study ECM regulation and mechanics.
  • She is embedded within the Groningen Research Institute for Asthma and COPD (GRIAC), contributing to interdisciplinary respiratory research.
  • Her work aims to identify ECM-driven mechanisms as therapeutic targets for lung diseases affecting large patient populations.
  • Dr. Burgess is actively involved in international scientific leadership, including chairing and speaking at major conferences such as the European Respiratory Society Lung Science Conference.
  • She has received multiple recognitions, including the Solbert Permutt Trailblazer Award (2025) and Fellowship of the American Thoracic Society (2021).
  • In addition to research, she contributes to education and mentorship in matrix biology and tissue regeneration at the graduate level.
  • This webinar is hosted co-hosted together with the International Society of Extracellular Matrix Pharmacology.

Dr. Diana Julie Leeming

  • Dr. Diana Julie Leeming is the Senior Director of Fibrosis, Hepatic, and Pulmonary Research at Nordic Bioscience.
  • She joined Nordic Bioscience in 2004 and assumed the role of Director of Fibrosis in 2010, later being promoted to Senior Director in 2024.
  • Dr. Leeming focuses on developing serologically assessed markers to evaluate extracellular matrix remodeling in patients with pulmonary or hepatic fibrosis, aiding in diagnosis and pharmacodynamic evaluation.
  • She is a principal inventor of the PRO-C3 assay, a fibrogenesis marker utilized in multiple clinical trial studies.
  • Dr. Leeming has authored over 280 peer-reviewed publications, demonstrating her extensive contributions to the field.
  • Her H-index is 69, her I10-index is 195, and her research has garnered over 15,736 citations as of February 2026.

Dr. Martin Pehrsson

  • Dr. Martin Pehrsson, a Senior Scientist and Scientific Alliance Manager working with Pulmonary Research at Nordic Bioscience.
  • He joined Nordic Bioscience in 2017, assumed the role of Senior Scientist in 2023 and Manager in 2025.
  • Dr. Martin Pehrsson focuses on the application of extracellular matrix remodeling biomarkers in clinical trials of patients with respiratory diseases, such as IPF and COPD, aiding in mode of action and pharmacodynamic evaluation.
  • He was part of the initial development of the CTX-III biomarker, a marker used to assess fibrosis resolution.
  • Dr. Martin Pehrsson has authored 38 peer-reviewed publications with an H- and i10-index of 8 and 287 citations as of April 2026

This webinar is hosted co-hosted together with the International Society of Extracellular Matrix Pharmacology.

FAP-cleaved Type III Collagen (C3F) is a Potential Marker for Intestinal Fibrosis in CD Patients

Fibroblast Activation Protein (FAP)-Cleaved Type III Collagen (C3F) is a Potential Marker for Intestinal Fibrosis in Patients with Crohn’s Disease

Introduction

Crohn’s disease (CD) is characterized by chronic inflammation in the gut, where severe complications such as fibrotic strictures require surgical resection. The stricture development involves excessive extracellular matrix (ECM) deposition due to continuous activation of intestinal myofibroblasts, that further contribute to instestinal fibrogenesis. Emerging data suggests that stricture-related intestinal myofibroblasts overexpress a serine protease called fibroblast activation protein (FAP). Furthermore, type III collagen deposition is increased during fibrosis in all layers of the intestinal tract, and studies have shown elevated collagen degradation in serum from patients with CD.

This study aimed to evaluate the potential of FAP-cleaved type III collagen (C3F) as a serum marker for intestinal fibrosis in CD.

Poster

Conclusion

C3F is elevated in patients with stenotic CD compared to luminal CD at baseline and remains elevated after surgical resection, suggesting that C3F reflects fibroblast activity during fibrostenosis and tissue remodeling following surgery. In patients with luminal CD, C3F levels were significantly higher, and early C3F levels (baseline, 3 months and 6 months) were significantly positively associated with ileal stenosis assessed at 12 months. This suggests that increased C3F may be predictive of future endoscopic disease activity or even a potential relapse.

Concluding, the findings of this study highlight the potential use of C3F as a novel biomarker for intestinal fibrosis in CD.

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