Canstatin, a type IV collagen fragment, is associated with risk of cardiovascular and all-cause mortality in patients with advanced atherosclerosis
Introduction
Atherosclerosis, a common underlying cause of cardiovascular disease, is defined by the formation of plaques in the arterial walls. Changes in the ECM composition impact the risk for plaque rupture, which may cause acute complications (i.e. stroke or myocardial infarction (MI)). Type IV collagen is primarily known as a major component of basement membranes and has previously been reported to promote plaque stability. Canstatin is the non-collagenous C-terminal domain of type IV collagen alpha 2 chain. It is not only a by-product of proteolytic activity, but also a bioactive molecule. This study investigated if canstatin was associated with adverse outcomes in patients with advanced carotid atherosclerosis.
Higher circulating canstatin levels in patients undergoing carotid endarterectomy predicted cardiovascular mortality and all-cause mortality over 7.5 years. This suggests that canstatin is a potential novel tool for risk stratification in patients with advanced atherosclerosis, warranting further studies.
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In this webinar we uncovered how the brain’s extracellular matrix (ECM) and emerging biomarkers are reshaping our understanding of neuroinflammation and neurodegeneration, with a focus on their role in disease mechanisms, diagnosis, and therapeutic innovation.
The brain is more than just neurons; it is a complex, finely tuned environment shaped by the extracellular matrix (ECM) and molecular signaling.
This webinar examines the structure and function of the brain ECM, emphasizing its influence on neural plasticity, signaling, and repair. After establishing a foundation in ECM biology, we will explore how this network interacts with disease mechanisms and why it has become a central focus in neuroscience.
Introductions and welcome to the webinar by moderator Dr. Signe Holm Nielsen
Fluid biomarkers for neurodegeneration and inflammation in neurological diseases– Prof. Dr. Ir. Charlotte Teunissen
Neuroinflammation, biomarkers and upcoming treatments in Multiple Sclerosis – Prof. Dr. Tobias Sejbæk
Should we target the Extracellular Matrix of the Brain in Drug discovery? – Dr. Kim Henriksen
Questions from the chat
Scientific Topics
A major topic will be the growing importance of biomarkers in neurodegenerative and neuroinflammatory disease research. Notably, phosphorylated tau at threonine 217 (pTau217) has emerged as a promising diagnostic marker for Alzheimer’s disease, representing a significant advance in early detection.
However, identifying equally robust and specific biomarkers for conditions such as Parkinson’s disease and multiple sclerosis remains challenging, with unresolved issues in diagnosis, prognosis, subtyping, and assessment of drug efficacy. The webinar will conclude by examining how insights into brain ECM dynamics and disease-specific molecular profiles can drive drug discovery and therapeutic innovation, offering new opportunities to develop targeted treatments and improve clinical outcomes.
Prof. Dr. Ir. Charlotte Teunissen
Prof. Dr. Ir. Charlotte Teunissen is a Full Professor of Neurochemistry dedicated to improving care for neurological disease patients through the development of body fluid biomarkers.
Her research spans the full biomarker development pipeline—from discovery to assay development, validation, and clinical implementation.
She leads the body fluid biomarker program at the Alzheimer Center Amsterdam, a key center for biomarker innovation in neurodegenerative diseases.
Prof. Teunissen’s work focuses on biomarkers for diagnosis, patient stratification, prognosis, and treatment monitoring in neurological conditions, particularly dementia.
She is an international leader in biomarker collaboration, serving as chair of the CSF Society and the Alzheimer’s Association Global Biomarker Standardization Consortium.
She recently co-founded the Coral proteomics consortium to advance proteomic approaches in biomarker research.
Prof. Teunissen coordinates the EU-funded Marie Curie MIRIADE project, training 15 early-stage researchers in dementia biomarker development.
Her team plays a critical role in translating biomarker research into clinical practice, with an emphasis on standardization and global accessibility.
She is recognized for fostering interdisciplinary and international collaborations to accelerate progress in neurodegenerative disease research.
Prof. Teunissen’s work is shaping the future of personalized neurology by enabling earlier diagnosis and more precise treatment of dementia and related disorders.
Dr. Kim Henriksen
Dr. Kim Henriksen is the Director of Endocrinology and Neuroscience at Nordic Bioscience, where he has worked since 2002 and assumed his current leadership role in 2018.
He leads a team of 15 scientists and technicians focused on developing novel biomarkers for neurodegenerative diseases, particularly blood-based tools for identifying individuals in need of treatment.
Dr. Henriksen’s research also targets the development of peptide therapies for metabolic diseases, including obesity, NASH, and type 2 diabetes.
He is a key inventor behind the DACRA peptide family, with the lead molecule currently in phase 2 clinical development.
His earlier work led to the patenting and advancement of two peptide families—KBPs and OXMs—now progressing toward clinical use.
Dr. Henriksen has authored nearly 200 peer-reviewed publications.
He has an H-index of 65, i10-index of 158, and over 11,985 citations as of August 2024.
His translational research bridges biomarker science and therapeutic innovation in both endocrinology and neuroscience.
Dr. Henriksen is widely recognized for his contributions to precision medicine in metabolic and neurodegenerative disorders.
He continues to drive Nordic Bioscience’s strategy in peptide drug development and biomarker discovery for complex chronic diseases.
Prof. Dr. Tobias Sejbæk
Dr. Tobias Sejbæk is Head of Research and Consultant in Neurology at Esbjerg Hospital, affiliated with the University of Southern Denmark.
He joined the University of Southern Denmark in 2011 and became Head of Research in 2019.
Dr. Sejbæk is a leading figure in clinical neurology, particularly in the field of multiple sclerosis (MS).
He serves as the national Principal Investigator for major MS clinical trials, including FENHANCE, GEMINI, HERCULES, and PERSEUS.
He has authored nearly 65 peer-reviewed publications and holds an H-index of 15.
Dr. Sejbæk has received multiple awards for his clinical trial presentations and contributions to advancing MS treatment.
He is a board member of the Danish Neurological Association, reflecting his national leadership in the neurology community.
His research focuses on translating clinical data into improved treatment strategies for neurological diseases.
He actively promotes evidence-based neurology and is committed to integrating new therapies into clinical practice.
Dr. Sejbæk continues to lead high-impact research and clinical initiatives that shape the future of MS care in Denmark and beyond.
We are also excited to inform you about our upcoming in-person event, The Extracellular Matrix Pharmacology Congress, taking place in Copenhagen in June 2026. This congress will be a unique opportunity to gather with leading experts in the field and explore the latest advancements in extracellular matrix research and pharmacology.
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.
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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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.
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 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.
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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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. The HS awareness week aims to spread knowledge about the disease and how it affects patients.
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.
If you want to find out more about how our biomarkers can be applied in Hidradenitis Suppurutiva, click on the button below.
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.
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.
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.
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)
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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