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Hemosiderin Accumulation in Liver Decreases Iron Availability in Tachycardia-Induced Porcine Congestive Heart Failure Model

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dc.abstract.enDespite advances in the management of iron deficiency in heart failure (HF), the mechanisms underlying the effects of treatment remain to be established. Iron distribution and metabolism in HF pathogenesis need to be clarified. We used a porcine tachycardia-induced cardiomyopathy model to find out how HF development influences hepatic and myocardial iron storing, focusing on ferritin, the main iron storage protein. We found that cumulative liver congestion (due to the decrease of heart function) overwhelms its capacity to recycle iron from erythrocytes. As a consequence, iron is trapped in the liver as poorly mobilized hemosiderin. What is more, the ferritin-bound Fe3+ (reflecting bioavailable iron stores), and assembled ferritin (reflecting ability to store iron) are decreased in HF progression in the liver. We demonstrate that while HF pigs show iron deficiency indices, erythropoiesis is enhanced. Renin–angiotensin–aldosterone system activation and hepatic hepcidin suppression might indicate stress erythropoiesisinduced in HF. Furthermore, assembled ferritin increases but ferritin-bound Fe3+ is reduced in myocardium, indicating that a failing heart increases the iron storage reserve but iron deficiency leads to a drop in myocardial iron stores. Together, HF in pigs leads to down-regulated iron bioavailability and reduced hepatic iron storage making iron unavailable for systemic/cardiac needs.
dc.affiliationWydział Medycyny Weterynaryjnej i Nauk o Zwierzętach
dc.affiliation.instituteKatedra Chorób Wewnętrznych i Diagnostyki
dc.contributor.authorKasztura, Monika
dc.contributor.authorKiczak, Liliana
dc.contributor.authorPasławska, Urszula
dc.contributor.authorBania, Jacek
dc.contributor.authorJaniszewski, Adrian
dc.contributor.authorTomaszek, Alicja
dc.contributor.authorZacharski, Maciej
dc.contributor.authorNoszczyk-Nowak, Agnieszka
dc.contributor.authorPasławski, Robert
dc.contributor.authorTabiś, Aleksandra
dc.contributor.authorKuropka, Piotr
dc.contributor.authorDzięgiel, Piotr
dc.contributor.authorPonikowski, Piotr
dc.date.access2026-03-06
dc.date.accessioned2026-03-06T09:21:51Z
dc.date.available2026-03-06T09:21:51Z
dc.date.copyright2022-01-18
dc.date.issued2022
dc.description.abstract<jats:p>Despite advances in the management of iron deficiency in heart failure (HF), the mechanisms underlying the effects of treatment remain to be established. Iron distribution and metabolism in HF pathogenesis need to be clarified. We used a porcine tachycardia-induced cardiomyopathy model to find out how HF development influences hepatic and myocardial iron storing, focusing on ferritin, the main iron storage protein. We found that cumulative liver congestion (due to the decrease of heart function) overwhelms its capacity to recycle iron from erythrocytes. As a consequence, iron is trapped in the liver as poorly mobilized hemosiderin. What is more, the ferritin-bound Fe3+ (reflecting bioavailable iron stores), and assembled ferritin (reflecting ability to store iron) are decreased in HF progression in the liver. We demonstrate that while HF pigs show iron deficiency indices, erythropoiesis is enhanced. Renin–angiotensin–aldosterone system activation and hepatic hepcidin suppression might indicate stress erythropoiesisinduced in HF. Furthermore, assembled ferritin increases but ferritin-bound Fe3+ is reduced in myocardium, indicating that a failing heart increases the iron storage reserve but iron deficiency leads to a drop in myocardial iron stores. Together, HF in pigs leads to down-regulated iron bioavailability and reduced hepatic iron storage making iron unavailable for systemic/cardiac needs.</jats:p>
dc.description.accesstimeat_publication
dc.description.bibliographyil., bibliogr.
dc.description.financepublication_nocost
dc.description.financecost0,00
dc.description.if5,6
dc.description.number3
dc.description.points140
dc.description.versionfinal_published
dc.description.volume23
dc.identifier.doi10.3390/ijms23031026
dc.identifier.eissn1422-0067
dc.identifier.issn1661-6596
dc.identifier.urihttps://sciencerep.up.poznan.pl/handle/item/7655
dc.identifier.weblinkhttps://www.mdpi.com/1422-0067/23/3/1026
dc.languageen
dc.relation.ispartofInternational Journal of Molecular Sciences
dc.relation.pagesart. 1026
dc.rightsCC-BY
dc.sciencecloudnosend
dc.share.typeOPEN_JOURNAL
dc.subject.enanimal model
dc.subject.eniron deficiency
dc.subject.enassembled ferritin
dc.subject.enferritin-bound Fe3+
dc.subject.enhepcidin
dc.titleHemosiderin Accumulation in Liver Decreases Iron Availability in Tachycardia-Induced Porcine Congestive Heart Failure Model
dc.typeJournalArticle
dspace.entity.typePublication
oaire.citation.issue3
oaire.citation.volume23