Month: May 2025

Type III and VI Collagen remodeling biomarkers have the potential to distinguish between IPF and HP

Introduction

IPF and HP are two ILDs with similar clinical phenotype but distinct management, making their precise separation critical. Serological biomarkers may assist in distinguishing the two. In this study we assessed the clinical value of type III and VI collagen remodeling biomarkers and their potential to act as a tool to distinguish between HP and IPF in two separate, independent cohorts.

Poster

Conclusion

We conclude that nordicPRO-C3™ could distinguish between HP and IPF in the AUH-ILD cohort. Furthermore, the distinct collagen remodeling takes place in each disease. In conclusion, these findings suggest that ECM remodeling biomarkers could act as potential tools to distinguish between HP and IPF.

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PRO-C3 and PRO-C6 fibrogenesis biomarkers in connective tissue disease-associated interstitial lung disease: results from the Phase IIb RECITAL trial

Introduction

ILD is a major cause of morbidity and mortality in connective tissue disease (CTD). Cyclophosphamide is an effective treatment for CTD-ILD, but is limited by side effects. Rituximab was tested as an alternative in the RECITAL phase IIb trial. The result was that both drugs improved lung function, but rituximab showed fewer adverse events.

The aim of this study was to evaluate the effect of cyclophosphamide and rituximab on fibrogenesis in CTD-ILD.

Poster

Conclusion

The decrease in nordicPRO-C6™ and nordicPRO-C3™ suggest that, besides their immunomodulatory effects, these drugs may also reduce fibrogenesis. Furthermore, nordicPRO-C3™ and nordicPRO-C6™, measured at baseline and as % change from baseline, are associated with FVC response. These findings highlight nordicPRO-C3™ and nordicPRO-C6™ as promising biomarkers for progressive CTD-ILD.

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Type III and VI collagen remodeling biomarkers have the potential to distinguish
between IPF and HP

Introduction

IPF and HP are two ILDs with similar clinical phenotype but distinct management, making their precise separation critical. Serological biomarkers may assist in this distinction. Extracellular matrix (ECM) remodeling is a hallmark of fibrosis. Collagen formation and degradation processes release peptide fragments into the blood that can be quantified by the nordicPRO-C3™ and nordicPRO-C6™ (type III and VI collagen formation), or the C3M and C6M (type III and VI collagen degradation) assays.

In this study we assessed the clinical value of Type III and VI collagen remodeling biomarkers and their potential to act as a tool to distinguish between HP and IPF in two separate, independent cohorts.

Poster

Conclusion

These findings suggest that ECM remodeling biomarkers such as nordicPRO-C3™ could act as potential tools to distinguish between HP and IPF.

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NordicPRO-C3™ and nordicPRO-C6™ fibrogenesis biomarkers in connective tissue disease-associated interstitial lung disease: results from the phase IIb RECITAL trial

Introduction

ILD is a major cause of morbidity and mortality in connective tissue disease (CTD). Cyclophosphamide is an effective treatment for CTD-ILD, but limited by side effects. In this study, we additionally tested rituximab as an alternative in the RECITAL phase IIb trial. Both drugs improved the lung function with rituximab showing fewer adverse events (Maher, 2022. Lancet Resp Med)

Poster

Conclusion

The decrease in nordicPRO-C3™ and nordicPRO-C6™ suggest that, besides their immunomodulatory effects, these drugs may also reduce fibrogenesis. Both biomarkers, measured at baseline and as % change from baseline, are associated with FVC response. These findings highlight nordicPRO-C3™ and nordicPRO-C6™ as promising biomarkers for progressive CTD-ILD.

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Identifying biomarkers of mild-stage emphysema in COPD patients via interpretable machine learning

Introduction

Emphysema results from alveolar damage—causing abnormal extracellular matrix (ECM) remodeling and impaired lung function. Early detection in mild, often asymptomatic stages is key to timely intervention. Although computed tomography (CT) scans are the most accurate detection method, pathological changes may occur before emphysema becomes visible, highlighting the need for non-invasive early detection approaches.

This study aimed to develop a proof-of-concept machine learning (ML) pipeline to identify patients with mild-stage emphysema using circulating biomarkers.

Poster

Conclusion

ML demonstrates potential for early-stage emphysema diagnosis through biomarker-driven methods. Quantifying fragments of ECM remodeling—driven by immune cell activity and collagen formation—could potentially serve as early diagnostic biomarkers in patients without lung function decline.

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Introduction

Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic and fatal lung disease with limited
treatment options. Fibroblast activation and ECM deposition is pivotal in development of IPF, thus
inhibiting fibrogenesis and ECM deposition is crucial for anti-fibrotic approaches to treat IPF.

This study aims to prove that tankyrase inhibition reduces fibrogenesis induced by a fibrotic cocktail (FC) in primary human lung fibroblasts derived from IPF patients and decreases extracellular matrix biomarkers nordicPRO-C3™ and nordicPRO-C6™.

Poster

Conclusion

These findings highlight the potential of tankyrase inhibiton as a therapeutic target for IPF and
support the use of the Scar–in-a-Jar model as an effective tool for IPF drug screening.

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Engineering liver fibrosis in a three-dimensional, extracellular matrix-hydrogel disease model

Introduction

Modeling fibrosis requires replicating the mechano-chemical cues of the extracellular matrix (ECM), including binding sites, three-dimensionality, and biomechanics. To engineer a liver fibrosis model based on native, decellularized ECM with spatial and compositional integrity, layered on a hydrogel of poly(ethylene glycol) diacrylate (PEGDA) that provides tunable mechanical properties.

This model aims to support cell recolonization and facilitate the investigation of cell-matrix interactions, fibrogenic remodeling, and therapeutic screening in a physiologically relevant context.

Poster

Conclusion

HSCs colonize porcine liver ECM and synthesize new collagen. Biochemical signaling and biomechanical properties drive ECM deposition, recapitulating key features of the fibrotic niche. Upon treatment with relaxin-2, HSCs display an ECM-degrading activity. The ECM-hydrogel constructs exhibit no cytotoxicity, and polymer concentration can be tuned to modulate the mechanical properties of the ECM. Due to its anatomical similarity to human tissue, porcine ECM offers a biologically relevant scaffold for in vitro fibrosis modeling without the ethical concerns associated with live animal use.

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Bile acids drive fibroblast activation, fibrogenesis, interstitial matrix fibrosis and outcomes in PSC

Introduction

Fibrosis often originates from a persistent insult that damages epithelial and endothelial cells and activates chronic pro-inflammatory processes that impair the regular course of tissue repair.

A hallmark of fibrosis is the activation of fibroblasts leading to excessive production of type I, III, and VI collagens in the interstitial space of the extracellular matrix (ECM). Several drivers, including transforming growth factor-beta (TGF-β), have been identified as key drivers of fibroblast activation. While bile acids (BA) have been shown to correlate with the fibroblast activation marker nordicPRO-C3™ in biliary diseases, their precise role in the process of fibrogenesis remains unclear.

The present work aims to investigate the relationship between bile acids and markers of ECM formation and degradation during anti-fibrotic therapy (an engineered FGF-19; NCT02704364 analogue;) and related prognostic ability of biomarkers reflecting fibroblast activity in PSC.

Poster

Conclusion

Fibroblast activation and collagen formation play a crucial role in determining outcomes in PSC. The data suggests that bile acids activate fibroblast driving fibrogenesis, and that lowering of bile acids attenuate the fibrotic drive. Lowering fibroblast activity may have positive effects on liver related outcomes in PSC.

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Weight dependent, weight independent and non-pharmacological effects on fibroblast activity in metabolic dysfunction associated steatotic liver disease (MASLD)

Introduction

It is well established that fibroblasts are activated by metabolic dysfunction and are a central component of liver function decline and death. Fibroblast activities, both type III and type VI collagen formation, have been shown to be highly prognostic for outcome of liver, heart and kidney related events in MAFLD populations. Fibroblast activity in man, may both be inhibited by weight dependent and independent
mechanisms, and as such monitoring fibroblast activities is essential.

Poster

Conclusion

Pharmacological and non-pharmacological induction of weight loss results in different deactivation of fibroblasts activities, which may have divergent efficacy on heart and liver related outcomes. Furthermore, weight dependent and independent mechanisms of deactivation fibroblasts may result in additional effects on bone and muscle. This understanding may be needed when designing the optimal intervention strategy, including possible combination regimens, for the individual MAFLD patient.

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PRO-C4, a biomarker of perisinusoidal fibrosis, is related to cardiometabolic risk factors, steatosis, and liver stiffness

Introduction

A histological characteristic of early liver damage is the formation of perisinusoidal fibrosis with thickening of the hepatocyte basement membrane. Type IV collagen is a key component of the basement membrane of the extracellular matrix and can be assessed serologically by the biomarker PRO-C4. Thus, PRO-C4 could potentially reflect early features of liver damage in patients with early-stage SLD.

In this study we aimed to explore whether basement membrane remodeling assessed systemically was related to risk factors of chronic liver disease including Met S, liver steatosis assessed by CAP and liver
stiffness by Fibroscan.

Poster

Conclusion

Elevated PRO-C4 is associated with presence of cardiometabolic risk factors and LSM>8kpa. PRO-C4 potentially reflects perisinusoidal fibrosis from early liver damage and repair due to its relation to increasing degree of steatosis. Furthermore, PRO-C4 was also related to elevated liver stiffness in a population at risk of SLD.

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