Title : The hypoferremic response to acute inflammation is maintained in thalassemia mice even under parenteral iron loading.

Pub. Date : 2021

PMID : 33987030






6 Functional Relationships(s)
Download
Sentence
Compound Name
Protein Name
Organism
1 Background: Hepcidin controls iron homeostasis by inducing the degradation of the iron efflux protein, ferroportin (FPN1), and subsequently reducing serum iron levels. Iron hepcidin antimicrobial peptide Mus musculus
2 Background: Hepcidin controls iron homeostasis by inducing the degradation of the iron efflux protein, ferroportin (FPN1), and subsequently reducing serum iron levels. Iron hepcidin antimicrobial peptide Mus musculus
3 Background: Hepcidin controls iron homeostasis by inducing the degradation of the iron efflux protein, ferroportin (FPN1), and subsequently reducing serum iron levels. Iron hepcidin antimicrobial peptide Mus musculus
4 Hepcidin expression is influenced by multiple factors, including iron stores, ineffective erythropoiesis, and inflammation. Iron hepcidin antimicrobial peptide Mus musculus
5 Despite the altered expression of the aforementioned hepcidin regulators, the stimulatory effect of LPS on hepcidin mRNA expression was blunt in iron-treated Hbbth3 /+ mice. Iron hepcidin antimicrobial peptide Mus musculus
6 Conclusion: Our study suggests that a hypoferremic response to LPS-induced acute inflammation is maintained in thalassemic mice with parenteral iron loading in a hepcidin-independent manner. Iron hepcidin antimicrobial peptide Mus musculus