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Real-world effectiveness and safety of bulevirtide monotherapy for up to 96 weeks in patients with HDV-related cirrhosis.
J Hepatol
January 2025
Division of Gastroenterology and Hepatology, Foundation IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy; CRC "A. M. and A. Migliavacca" Center for Liver Disease, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy; D-SOLVE consortium, an EU Horizon Europe funded project (No 101057917). Electronic address:
Background And Aims: Bulevirtide (BLV) 2 mg/day is EMA approved for treatment of compensated chronic hepatitis due to Delta virus (HDV) infection, however real-life data in large cohorts of patients with cirrhosis are lacking.
Methods: Consecutive HDV-infected patients with cirrhosis starting BLV 2 mg/day since September 2019 were included in a European retrospective multicenter real-life study (SAVE-D). Patient characteristics before and during BLV treatment were collected.
Hemojuvelin-mediated hepcidin induction requires both bone morphogenetic protein type I receptors ALK2 and ALK3.
Blood Adv
June 2024
Department of Anesthesiology, Goethe University Frankfurt, Intensive Care Medicine and Pain Therapy, University Hospital Frankfurt, Frankfurt, Germany.
Hemojuvelin (HJV) is a glycosylphosphatidylinositol-anchored protein of the repulsive guidance molecule family acting as a bone morphogenetic protein (BMP) coreceptor to induce the hepatic iron regulatory protein hepcidin. Hepcidin causes ubiquitination and degradation of the sole known iron exporter ferroportin, thereby limiting iron availability. The detailed signaling mechanism of HJV in vivo has yet to be investigated.
View Article and Find Full Text PDFA functional interplay between the two BMP-SMAD pathway inhibitors TMPRSS6 and FKBP12 regulates expression in vivo.
Am J Physiol Gastrointest Liver Physiol
March 2024
Division of Genetics and Cell Biology, IRCCS Ospedale San Raffaele, Milan, Italy.
The Activin A Receptor type I (ALK2) is a critical component of BMP-SMAD signaling that, in the presence of ligands, phosphorylates cytosolic SMAD1/5/8 and modulates important biological processes, including bone formation and iron metabolism. In hepatocytes, the BMP-SMAD pathway controls the expression of , the liver peptide hormone that regulates body iron homeostasis via the BMP receptors ALK2 and ALK3, and the hemochromatosis proteins. The main negative regulator of the pathway in the liver is transmembrane serine protease 6 (TMPRSS6), which downregulates by cleaving the BMP coreceptor hemojuvelin.
View Article and Find Full Text PDFAuthor Correction: Consensus Statement on the definition and classification of metabolic hyperferritinaemia.
Nat Rev Endocrinol
March 2024
Department of Medicine I, Medical University of Innsbruck, Innsbruck, Austria.
Iron homeostasis in mice: does liver lobe matter?
Am J Physiol Gastrointest Liver Physiol
November 2023
Department of Pediatric Oncology, Hematology and Immunology and Hopp Children Cancer Center (KiTZ), University Hospital Heidelberg, Heidelberg, Germany.
The liver plays a crucial role in maintaining systemic iron homeostasis through iron storage, sensing of systemic iron needs, and production of the iron-regulatory hormone hepcidin. While mice are commonly used as models for studying human iron homeostasis, their liver structure differs significantly from humans. Since the mouse liver is structured in six separated lobes, often, the analysis of a single defined lobe is preferred due to concerns over data reproducibility between experimental cohorts.
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