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Editorial: Extracellular Matrix Biomarkers Illuminate the Architecture of Portal Hypertension in End-Stage Liver Disease-Authors’ Reply.
March 1, 2026
Aliment Pharmacol Ther
March 1, 2026
Aliment Pharmacol Ther
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March 1, 2026
Aliment Pharmacol Ther
Abstract BACKGROUND Extracellular matrix (ECM) remodelling in advanced chronic liver disease (ACLD) is characterised by hepatic fibrosis and (sinusoidal) basement membrane development contributing to portal hypertension (PH) and clinical complications. METHODS Patients with stable ACLD (n = 232) undergoing hepatic venous pressure gradient (HVPG) measurement were included. Blood biomarkers reflecting fibrosis formation (PRO-C3, PRO-C6, PRO-C4 and PRO-C18L) […]
March 1, 2026
Osteoarthr Cartil Open
Abstract OBJECTIVE To explore associations between patient-reported pain outcomes and knee osteoarthritis (OA) subtypes based on systemic biochemical markers and joint structural pathology as defined by MRI. METHODS Data were obtained from 297 knee OA patients from the IMI-APPROACH study. Pain outcomes were assessed using the KOOS, WOMAC, ICOAP, NRS, PainDETECT, and a pain diary. […]
March 1, 2026
Aliment Pharmacol Ther
Abstract BACKGROUND Extracellular matrix (ECM) remodelling in advanced chronic liver disease (ACLD) is characterised by hepatic fibrosis and (sinusoidal) basement membrane development contributing to portal hypertension (PH) and clinical complications. METHODS Patients with stable ACLD (n = 232) undergoing hepatic venous pressure gradient (HVPG) measurement were included. Blood biomarkers reflecting fibrosis formation (PRO-C3, PRO-C6, PRO-C4 and PRO-C18L) […]
February 24, 2026
Osteoarthritis Cartilage
Abstract OBJECTIVE To evaluate the association of neoepitopes from type I and II collagen with knee osteoarthritis (OA) progression phenotypes using data from the OA-FNIH biomarker consortium, with comparison to associations of the other biomarkers assessed in this sample during the consortium’s phase 1 analysis. DESIGN Serum (s) and urinary (u) neoepitopes of type I […]
February 23, 2026
Geroscience
Abstract Although interest in biomarkers of biological aging is growing, consensus on reliable, non-invasive indicators remains limited. Endotrophin, a bioactive fragment released during collagen type VI formation, reflects fibroblast activation and extracellular matrix remodeling and has been linked to chronic diseases, metabolic dysfunction, and inflammation. Whether circulating endotrophin also captures aging-related phenotypes and mortality risk in […]
February 16, 2026
J Gastroenterol Hepatol
Abstract BACKGROUND Noninvasive fibrosis testing is crucial for metabolic dysfunction-associated steatotic liver disease (MASLD) management. This study evaluated a marker of activated mesenchymal fibrogenic cells, circulating fibroblast activation protein (cFAP), in a novel diagnostic algorithm, FAP Index, for patients with MASLD. METHODS Two retrospective cohorts recruited from tertiary hepatology clinics were studied as training (n = 160) […]
February 1, 2026
Annu Rev Physiol
Abstract Cardiorenal syndrome (CRS) represents a complex interplay of pathophysiological processes that create a self-perpetuating cycle of heart and kidney dysfunction. While it is clearly understood how hemodynamic changes connect pathogenesis in the two organs, other processes are also in play. Some are the structural changes involving both the cellular and extracellular compartments that precede […]
February 1, 2026
Am J Physiol Cell Physiol
Abstract Endotrophin, a biologically active fragment derived from the α3 chain of collagen type VI, has emerged as both a risk biomarker and a potential pathogenic factor in cardiovascular-kidney-metabolic (CKM) syndrome. Over the past decade, research has shed light on its role in various noncommunicable diseases, emphasizing its signaling properties and diagnostic potential. Despite these […]
February 1, 2026
Am J Physiol Heart Circ Physiol
Abstract Wound healing after myocardial infarction (MI) is a dynamic and multifaceted process that links the molecular alterations induced by or in response to prolonged ischemia with structural and physiological changes to the damaged myocardium. Changes, at the tissue level, are driven by a complex intersection of cellular and molecular mechanisms that operate along a […]