Structural and functional abnormalities in iron-depleted heart

Kobak, Kamil; Radwańska, Malwina; Dzięgała, Magdalena; Kasztura, Monika; Josiak, Krystian; Banasiak, Waldemar; Ponikowski, Piotr; Jankowska, Ewa A.

doi:10.1007/s10741-018-9738-4

Cited by 41 publications

(42 citation statements)

References 75 publications

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“…Relative heart and spleen weight showed a strong positive correlation to serum transferrin levels (heart: R = 0.78, p < 0.01; spleen: R = 0.74, p < 0.01). This is in line with previous findings indicating that a Fe-deficient diet induced cardiomegaly with concomitant anemia [60] and splenomegaly in mice. [61] Interestingly, in the latter study Gibson et al [61] fed a diet with lower Fe amounts (3 mg kg −1 ) and for a longer feeding period (17 weeks) after weaning as done herein.…”

Section: Discussionsupporting

confidence: 93%

Effects of a Cumulative, Suboptimal Supply of Multiple Trace Elements in Mice: Trace Element Status, Genomic Stability, Inflammation, and Epigenetics

Finke

Winkelbeiner

Lossow

et al. 2020

Molecular Nutrition Food Res

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Scope: Trace element (TE) deficiencies often occur accumulated, as nutritional intake is inadequate for several TEs, concurrently. Therefore, the impact of a suboptimal supply of iron, zinc, copper, iodine, and selenium on the TE status, health parameters, epigenetics, and genomic stability in mice are studied. Methods and results: Male mice receive reduced or adequate amounts of TEs for 9 weeks. The TE status is analyzed mass-spectrometrically in serum and different tissues. Furthermore, gene and protein expression of TE biomarkers are assessed with focus on liver. Iron concentrations are most sensitive toward a reduced supply indicated by increased serum transferrin levels and altered hepatic expression of iron-related genes. Reduced TE supply results in smaller weight gain but higher spleen and heart weights. Additionally, inflammatory mediators in serum and liver are increased together with hepatic genomic instability. However, global DNA (hydroxy)methylation is unaffected by the TE modulation. Conclusion: Despite homeostatic regulation of most TEs in response to a low intake, this condition still has substantial effects on health parameters. It appears that the liver and immune system react particularly sensitive toward changes in TE intake. The reduced Fe status might be the primary driver for the observed effects.

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Section: Discussionsupporting

confidence: 93%

Effects of a Cumulative, Suboptimal Supply of Multiple Trace Elements in Mice: Trace Element Status, Genomic Stability, Inflammation, and Epigenetics

Finke

Winkelbeiner

Lossow

et al. 2020

Molecular Nutrition Food Res

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“…However, the mechanisms underlying such benefits remain controversial 7,8 . Different in vitro studies showed detrimental effects of ID on mitochondrial function among myoblasts and cardiomyocytes 9,10 . Iron treatment has been associated with improved muscular energetics in patients with HF 11 .…”

Section: Introductionmentioning

confidence: 99%

Short‐term changes in left and right systolic function following ferric carboxymaltose: a substudy of the Myocardial‐IRON trial

et al. 2020

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Aims The mechanisms underlying the beneficial effect of ferric carboxymaltose (FCM) in patients with heart failure (HF) and iron deficiency (ID) have not been completely characterized. The Myocardial-IRON trial was a double-blind, randomized trial that evaluated myocardial iron repletion following FCM vs. placebo in 53 patients with HF and ID. In this post hoc analysis, we evaluated whether treatment with FCM was associated with cardiac magnetic resonance changes in left and right ventricular function (LVEF and RVEF, respectively) at different points of systolic dysfunction. Methods and results We included patients from the Myocardial-IRON trial with left and right ventricular systolic dysfunction (LVSD and RVSD, respectively) at enrolment. Linear mixed regression models were used to evaluate changes at 7 and 30 days on LVEF and RVEF at cardiac magnetic resonance. At enrolment, 27 (50.9%) and 38 (71.7%) patients had LVEF < 40% (LVSD 1) or <45% (LVSD 2), respectively, and 10 (18.9%) and 17 (32.1%) patients had RVEF < 45% (RVSD 1) or <51% in women and <52% in men (RVSD 2) , respectively. Treatment with FCM was associated with a significant improvement in LVEF at 30 days (LVSD 1 : Δ2.3%, P < 0.001; LVSD 2 : Δ4.1, P = 0.014). FCM was also associated with a significant and early improvement in RVEF at 7 days (RVSD 1 : Δ6.9%, P = 0.003; RVSD 2 : Δ3.2%, P = 0.003) that persisted at 30 days (RVSD 1 : Δ8.1%, P < 0.001; RVSD 2 : Δ4.7%, P < 0.001). Conclusions In patients with HF and systolic dysfunction with ID, FCM was associated with short-term improvement in LVEF and, especially, in RVEF.

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“…В связи с существенной ролью железа в многочисленных процессах (обеспечение нормальной функции клетки, энергетический обмен, передача клеточного сигнала, экспрессия генов, регуляция клеточного роста и дифференцировки [44]) в последнее время пристальное внимание уделяется изучению его содержания и функции в миокарде. На основании определения содержания железа в сердечной мышце появился даже термин «миокардиальный ЖД» (МЖД), который не всегда зависим от системного ЖД и тем более от наличия и выраженности анемии [82]. V. Melenovsky с соавт.…”

Section: патофизиологические последствия анемии и железодефицитаunclassified

Anaemia and iron deficiency in chronic heart failure patients

et al. 2019

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Tis review focused on prevalence of anemia and iron defciency (ID) in CHF and their eﬀect on the course and prognosis of this condition. Based on evaluation of numerous laboratory data defnitions of anemia and ID were suggested. Specifcally, a diagnostic value of measuring serum iron, serum ferritin, transferrin saturation, total iron-binding capacity, and concentration of soluble transferrin receptors was discussed. Te review highlighted the importance of measuring bone marrow iron, which is rarely used in everyday clinical practice even though this test is considered a «gold standard» of ID diagnosis. Te review provided an insight into pathogenetic mechanisms of ID in CHF including insufcient iron supply, role of inﬂammation, erythropoietin, RAS, and eﬀects of some pharmacological therapies. Te authors described physiological consequences of ID and anemia, activation of hemodynamic and non-hemodynamic compensatory mechanisms, which develop in response to anemia and not infrequently aggravate CHF. Special atention was paid to current approaches to treatment of anemia and ID in CHF, including a discussion of efcacy and safety of oral and intravenous dosage forms of iron and hemopoiesis stimulators.

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Structural and functional abnormalities in iron-depleted heart

Cited by 41 publications

References 75 publications

Effects of a Cumulative, Suboptimal Supply of Multiple Trace Elements in Mice: Trace Element Status, Genomic Stability, Inflammation, and Epigenetics

Effects of a Cumulative, Suboptimal Supply of Multiple Trace Elements in Mice: Trace Element Status, Genomic Stability, Inflammation, and Epigenetics

Short‐term changes in left and right systolic function following ferric carboxymaltose: a substudy of the Myocardial‐IRON trial

Anaemia and iron deficiency in chronic heart failure patients

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