Iron Matryoshka—Haemochromatosis nested in Ferroportin Disease? [PDF]
Liver International, 2019 See Article on Page ...
André Viveiros +3 more
openaire +2 more sources
Increased calcification by erythrophagocytosis in aortic valvular interstitial cells
ESC Heart Failure, Volume 12, Issue 2, Page 1469-1473, April 2025.Abstract Background Calcific aortic valve disease (CAVD) progresses over time to severe aortic stenosis and eventually heart failure. Recent evidence indicates that intraleaflet haemorrhage (ILH) strongly promotes CAVD progression. However, it remains poorly understood how it mechanistically contributes to valvular calcification.
Zihan Qin +3 more
wiley +1 more source
Expression of an innate immune element (mouse hepcidin-1) in baculovirus expression system and the comparison of its function with synthetic human hepcidin-25 [PDF]
, 2011 Hepcidin is an innate immune element which decreases the iron absorption from diet and iron releasing from macrophage cell. In contrast to the chemical iron chelators, there has been limited effort applied to the specific use of hepcidin as a new drug ...
Alimohammadian, M. +5 more
core +1 more source
Iron Status and Analysis of Efficacy and Safety of Ferric Carboxymaltose Treatment in Patients with Inflammatory Bowel Disease [PDF]
, 2012 Background and Aims:We analyzed iron deficiency and the therapeutic response following intravenous ferric carboxymaltose in a large single-center inflammatory bowel disease (IBD) cohort.
Anker SD +45 more
core +1 more source
The flatiron mutation in mouse ferroportin acts as a dominant negative to cause ferroportin disease
Blood, 2007 Abstract Ferroportin disease is caused by mutation of one allele of the iron exporter ferroportin (Fpn/IREG1/Slc40a1/MTP1). All reported human mutations are missense mutations and heterozygous null mutations in mouse Fpn do not recapitulate the human disease. Here we describe the flatiron (ffe) mouse with a missense mutation (H32R) in
Irene E, Zohn +8 more
openaire +3 more sources
Pharmacological Targeting of the Hepcidin/Ferroportin Axis [PDF]
Frontiers in Pharmacology, 2016 The iron regulatory hormone hepcidin limits iron fluxes to the bloodstream by promoting degradation of the iron exporter ferroportin in target cells. Hepcidin insufficiency causes hyperabsorption of dietary iron, hyperferremia and tissue iron overload, which are hallmarks of hereditary hemochromatosis.
Sebastiani, Giada +2 more
openaire +2 more sources
The role of iron in normal and impaired testicular function
Andrology, EarlyView.Abstract Iron plays a critical role in testicular physiology, impacting spermatogenesis, testosterone production, and overall testicular function. Iron homeostasis is maintained through systemic and cellular regulatory mechanisms, including hepcidin‐mediated systemic iron control and the iron‐responsive element/iron regulatory protein (IRE/IRP) system ...
Aileen Harrer +2 more
wiley +1 more source
Membrane Transporters Involved in Iron Trafficking: Physiological and Pathological Aspects
Biomolecules, 2023 Iron is an essential transition metal for its involvement in several crucial biological functions, the most notable being oxygen storage and transport. Due to its high reactivity and potential toxicity, intracellular and extracellular iron levels must be
Andrea Pasquadibisceglie +3 more
doaj +1 more source
Novel mutation in addition to functional TMPRSS6 gene polymorphisms originate an IRIDA-like phenotype in an African child [PDF]
, 2019 Iron-refractory iron deficiency anemia (IRIDA) is a rare autosomal recessive anemia often unresponsive to oral iron intake and partially responsive to parenteral iron treatment. The disease originates from mutations in TMPRSS6 gene, encoding Matriptase 2,
Batalha, Sara +7 more
core
Transition metal ions at the crossroads of mucosal immunity and microbial pathogenesis. [PDF]
, 2014 Transition metal ions are essential micronutrients for all living organisms. In mammals, these ions are often protein-bound and sequestered within cells, limiting their availability to microbes. Moreover, in response to infection, mammalian hosts further
Diaz-Ochoa, Vladimir E +3 more
core +2 more sources