Collagen Type I Degradation Biomarkers Are Associated with Risk of Mortality After STEMI

Collagen type I degradation biomarkers are associated with risk of mortality after ST-elevated
myocardial infarction.

Introduction

Following ST-elevation myocardial infarction (STEMI), there is acute degradation of type I collagen (COL1), the primary structural protein of the myocardium. This process reflects extensive extracellular matrix remodeling, which may contribute to cardiac tissue destabilization and elevate the risk of subsequent adverse events. To better understand this pathological remodeling, we aimed to quantify COL1 using specific plasma biomarkers, including a novel signaling fragment of COL1 (C1SIG) and a more established COL1 degradation marker (C1M). Additionally, we investigated the prognostic value of these biomarkers for predicting all-cause mortality following a STEMI event.

Poster

Conclusion

C1M and C1SIG are independently prognostic for mortality in STEMI patients after 1 year, in a multivariate
model based on the Framingham Score. Assessing acute extracellular matrix processing in STEMI patients
using COL1 biomarkers could be beneficial for predicting mortality and identifying a patient subset at
increased risk of long-term outcome.

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    ACR70 Response and Its Dependence on Deep Tissue Efficacy

    Introduction

    Over the past decade, drugs developed for rheumatoid arthritis (RA) have been approved based on an ACR20 response rate of 60%. There is an increasing need for new RA drugs to achieve an ACR100 response in a significant portion of patients. Achieving ACR100 can profoundly improve patients’ quality of life by reducing pain, enhancing physical function, and decreasing fatigue.

    The key question remains: which patients are likely to achieve ACR100?

    An important aspect of RA pathogenesis involves the destruction and remodeling of bone, cartilage, and synovial tissue. Serum biomarkers that measure collagen and other extracellular matrix fragments can be used to assess disease activity at the tissue level. Examples include C1M (type I collagen destruction), C4M (type IV collagen destruction), and Osteocalcin (bone formation) [1].

    The aim of this study was to examine the demographic, clinical, and serum markers of tissue remodeling as predictors linked to ACR20, ACR50 and ACR70 responses to tocilizumab.

    Poster

    Conclusion

    While predictors of moderate response (ACR20) included clinical, demographic, and biomarker factors, predictors of significant response (ACR70) were exclusively biomarkers of extracellular matrix fragmentation. To achieve remission (ACR70 or ACR100) may require therapeutic interventions that specifically target and address tissue remodeling processes.

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      Serological Extracellular Matrix Fragments May Serve as Early Kidney Damage Biomarkers

      Serological extracellular matrix fragments may serve as early kidney damage biomarkers in children with defects in Alport genes

      Introduction

      Alport syndrome is a genetic disorder caused by variants in COL4A3, COL4A4, or COL4A5, which encode type IV collagen. The α3.α4.α5(IV) collagen network is a critical structural component of the glomerular and tubular basement membranes within the kidney’s extracellular matrix (ECM). Variants in this network compromise basement membrane integrity, leading to cell injury, inflammation, and fibrotic remodeling of the surrounding interstitial matrix, which contributes to progressive kidney dysfunction.

      We aim to identify serological protease-generated fragments of the ECM as potential early biomarkers of kidney damage.

      Poster

      Conclusion

      The following biomarkers were altered in children with Alport syndrome, compared to healthy donors, before the onset of detectable proteinuria:


      These biomarkers could potentially indicate early kidney damage and enable earlier initiation of kidney-protective treatments in children with Alport syndrome.

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        Hidradenitis Suppurutiva Awareness Week: Biomarkers for Hidradenitis Suppurutiva

        The Hidradenitis Suppurutiva Awareness Week is held annually to spread knowledge about the disease and how it affects patients. Affecting roughly 1% of the population, HS causes significant physical and emotional challenges that are often overlooked.

        Hidradenitis Suppurativa Awareness Week is held annually to raise awareness about this systemic skin disease

        HS is believed to result from a complex mix of genetic predisposition, lifestyle factors, and immune system dysfunction, driving a continuous cycle of inflammation. It commonly presents as painful nodules, abscesses, draining tunnels beneath the skin, and scarring.

        These symptoms often cause physical discomfort and disability, affecting quality of life, personal relationships, and career opportunities. People living with HS respond differently to treatments, and we believe that raising awareness and supporting research is key to developing tailored treatment strategies that truly address their challenges.

        Our dermatology biomarkers enable precision medicine by providing information about ongoing pathological processes, such as damage and repair, within the ECM. This can guide targeted treatments and therapies, enhancing patient outcomes and personalized medicine approaches. At the same time, our markers, supported by our long history of experience and expertise, expedite drug development by specifically identifying target populations and reducing costs, over proteomic providers’ hopes to hit the right target by chance.

        Type III and VI Collagen Have the Potential to Distinguish Between IPF and HP

        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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          NordicPRO-C3™NordicPRO-C6™ in CTD-ILD: Results From the Phase IIb RECITAL Trial

          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’ Potential to Distinguish Between IPF and HP

            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™ in Connective Tissue Disease-Associated Interstitial Lung Disease

              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 Patients with Mild-Stage Emphysema in COPD via Machine Learning

                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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                  Tankyrase Inhibitor OM153 Exhibits Anti-Fibrotic Effects in a Scar-in-a-Jar Pulmonary Fibrosis Model

                  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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