Month: August 2026

The fibroblast activity biomarkers, PRO-C11, quantified in serum, is associated with disease activity and treatment response in patients with hidradenitis suppurativa

Introduction

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by inflammatory nodules, abscesses and sinus tracts. A key pathological feature is fibrosis, which is caused by accumulation of extracellular matrix (ECM) proteins. Type XI collagen is a minor fibrillar collagen, produced by dermal fibroblasts, and are upregulated in skin fibrosis. This study investigated the relationship between the serological biomarker PRO-C11, quantifying type XI  collagen formation, with disease severity and treatment response in HS patients.

Poster

Conclusion

The serum biomarker PRO-C11 was associated with disease severity in patients with HS, and mildly associated with IHS 4 improvement after 3-6 months of anti TNF α treatment. Such biomarker may serve as objective measures of fibrosis and tissue remodeling in HS, help identifying patients at risk of disease progression and the evaluation of treatment response.

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Clinically validated markers of extracellular matrix remodeling are altered by anti-fibrotic compounds in a human skin ex vivo model

Introduction

Skin pathologies, such as hidradenitis suppurativa and scleroderma, are characterized by excessive extracellular matrix (ECM) remodeling. Clinically validated ECM neo-epitope biomarkers, related to progression, treatment response, and outcomes, may be useful for the evaluation of potential anti-inflammatory and anti-fibrotic effects.

Poster

Conclusion

This study found that an MMP-inhibitor and anti-fibrotic decreased biomarkers of ECM remodeling in a human skin ex vivo model and may potentially be used as a tool for evaluating anti-inflammatory and anti-fibrotic compounds in a 3D skin structure.

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Early changes in serum PRO-C6 predict lung function trajectories in idiopathic pulmonary fibrosis

Introduction

Extracellular matrix remodeling is central to idiopathic pulmonary fibrosis (IPF) pathology and progression. Especially remodeling of type VI collagen (COL6) has been linked to disease severity and progression. COL6 synthesis releases the neoepitope PRO-C6, which includes the signaling peptide endotrophin, that has pro-fibrotic effects and may bind to and activate platelets. Thus, serum PRO-C6 may be a candidate surrogate endpoint in clinical trials of IPF. Currently, there are no reliable tools to predict lung function trajectories.

The aim of this study was to evaluate the prognostic ability of assessing early changes in serum PRO-C6 for predicting future lung function trajectories in IPF.

Poster

Conclusion

This study found that increases in serum PRO-C6 were prognostic for future FVC decline, suggesting that PRO-C6 dynamics may identify high risk patients and could be a surrogate endpoint in clinical trials and a tool to improve patient care.

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Biomarkers of collagen turnover and immune cell activity distinguish fibrotic hypersensitivity pneumonitis from idiopathic pulmonary fibrosis

Introduction

Idiopathic pulmonary fibrosis (IPF) is the most common cause of pulmonary fibrosis (PF), although it is also present in other interstitial lung diseases (ILDs). This includes hypersensitivity pneumonitis (HP), which is an inflammatory disease caused by an exacerbated response to environmental antigens and can be classified into fibrotic (fHP) or non-fibrotic (non-fHP). Due to the various differences between IPF and fHP, tools to aid the distinction are needed.

This study aimed to assess tissue remodeling and immune cell activity biomarkers as potential tools to distinguish between HP phenotypes and IPF.

Poster

Conclusion

The findings of this study are reflective of the different pathophysiological characteristics underlying each disease and highlights the potential of non-invasive serological biomarkers collagen and immune cell activity as potential tools to distinguish between HP and IPF in the clinic.

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Dynamic changes in type III collagen formation and degradation are associated with fibrotic activity following hepatic injury in rats

Introduction

Non-invasive biomarkers of collagen turnover enable assessment of drug effects on the extracellular matrix. Type III collagen formation (fibrogenesis) and degradation (fibrolysis) can be measured with
nordicPRO-C3™ and nordicCTX-III™, respectively. A shift toward fibrolysis has recently been associated with improvement of hepatic fibrosis in patients with metabolic dysfunction-associated steatohepatitis (MASH), making PRO-C3 and CTX-III relevant biomarkers for translational studies of hepatic fibrosis.
I this study, rodent versions of CTX-III (rCTX-III) and PRO-C3 (rPRO-C3) were developed and applied in two preclinical models of hepatic fibrosis.

Poster

Conclusion

In this study we developed robust assays for the rodent fibrolysis biomarker rCTX-III and fibrogenesis biomarker rPRO-C3. The biomarkers were applied in two hepatic fibrosis rat models, showing increased
type III collagen turnover after injury. In conclusion, rCTX-III and rPRO-C3 may serve as translational biomarkers in antifibrotic drug development.

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ADAPT and VCTE show comparable performance for identifying MASH patients with significant fibrosis: Implications for selecting patients eligible for therapy

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of liver-related morbidity and mortality, with fibrosis stage being the strongest predictor of adverse outcomes. Following the recent approval of pharmacological therapies for metabolic dysfunction–associated steatohepatitis (MASH) in patients with moderate fibrosis (F2–F3) without cirrhosis (F4), there is an urgent need for reliable non-invasive tests (NITs) to identify patients eligible for therapy. The ADAPT algorithm, incorporating the serum biomarker PRO-C3, along with platelets, age, and diabetes status, has recently transitioned to the Roche Cobas® e801 high throughout IVD analyzer.

This study evaluated the diagnostic performance of two well-established NITs for fibrosis assessment – the PRO-C3-based ADAPT algorithm and vibration-controlled transient elastography (VCTE) for identifying F2-3, F3-4 or F4 patients in a Danish prospective outpatient cohort.

Poster

Conclusion

ADAPT and VCTE performed similarly in detecting F2-F3, F3-4 fibrosis or F4 cirrhosis, one being blood-based and the other imaging-based. As many F2-F3 cases are missed, this indicates a large number of patients may be left untreated using only one text. These findings support further investigating of NITs for non-invasive fibrosis assessment and for identifying patients eligible for MASH therapy.

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VICM, a biomarker of macrophage-driven inflammation, as a risk marker of kidney disease progression in people with type 2 diabetes

Introduction

Hyperglycemia-induced metabolic stress promotes macrophage recruitment, driving inflammation, fibrosis, and kidney damage. Early biomarkers that can serve as risk markers for progression of diabetic kidney disease (DKD) are needed. We investigated whether circulating VICM—a fragment of citrullinated, MMP-degraded vimentin—is a risk marker for progression of DKD in people with type 2 diabetes (T2D) and moderately increased albuminuria.

Poster

Conclusion

Higher VICM is an independent risk marker of DKD progression in people with T2D. Biomarkers reflecting macrophage-driven immune dysregulation, such as VICM, may enable early identification of people at high risk of kidney complications.

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Collagen Turnover and Fibrogenesis Biomarkers Associate with Kidney Disease Progression in CKD: Data from CRIC and NURTuRE-CKD

Introduction

Fibrosis is a central pathogenic process in CKD progression, and biomarkers reflecting this process may offer prognostic value. Circulating PRO-C6, a pro-fibrotic signaling and tissue formation fragment of type VI collagen, and urinary C3M, an immune cell-mediated degradation fragment of type III collagen, have been previously explored in CKD cohorts, showing prognostic value in patients with different etiologies. The aim of this study was to validate the prognostic potential of PRO-C6 and uC3M in two large well-characterized, prospective, multicenter non-dialysis CKD cohorts.

Poster

Conclusion

Increased circulating PRO-C6 and decreased urinary C3M are independently associated with kidney disease progression and a more rapid decline in eGFR. Increased circulating PRO-C6 is also associated with risk of death. PRO-C6 and C3M provide mechanistic insights into collagen remodeling and fibrogenesis processes during CKD progression that are not captured by conventional markers of kidney function such as eGFR and UACR and kidney injury markers.

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Recurrence of atrial fibrillation is reflected by elevated formation of collagen type III and VI after ablation treatment

Introduction

Catheter ablation treatment for atrial fibrillation (AF) induces controlled myocardial injury to the pulmonary veins. This targeted injury initiates a wound healing response involving inflammation, fibroblast activation, and ECM remodeling. Collagen type III remodeling, deposited early during tissue repair, and type VI, which supports ECM organization, may indicate a persistent wound healing response rather than physiological scar formation.

The aim of this study was to investigate changes in circulating biomarkers of collagen III formation and collagen VI turnover in individuals with AF that underwent ablation to characterize the ECM remodeling response and explore their potential as indicators of post-procedural fibrosis.

Poster

Conclusion

The findings of this study suggest that PRO-C3 and PRO-C6 may reflect excessive activation of fibroblasts
following the ablation, and although physiological scarring is necessary, AF recurrence might
be driven by overactive fibrosis. These biomarkers could therefore potentially assist in identifying
patients who develop excessive scarring and could benefit from antifibrotic treatment after their
ablation therapy.

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Naturally occurring COL1 fragments induce COL3 formation in 3D PEG hydrogel model with human ventricular cardiac fibroblasts

Introduction

Cardiac fibrosis is a feature of many cardiovascular diseases and is characterized by activation of cardiac fibroblasts. COL3 is one of the ECM proteins affected early during the myocardial fibrotic process and contributes to increased tissue stiffness. Certain COL1 peptide sequence motifs have been observed to stimulate collagen formation or degradation. This project examines the effects of nine of the most abundant naturally occurring urinary COL1 derived peptides on COL3 turnover in a 3D in vitro cardiac fibroblast model.

Poster

Conclusion

Naturally occurring COL1-derived peptides induced a pro fibrotic response in cardiac fibroblasts, resulting in increased COL3 synthesis. These findings suggest that COL1 fragments may contribute to cardiac ECM remodeling and warrant further investigation in fibrosis-related cardiomyopathies.

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