Serum Hepcidin-20 is Elevated during the Acute Phase of Myocardial Infarction

Suzuki, Hiroshi; Toba, Kenji; Kato, Kiminori; Ozawa, Tomohiro; Tomosugi, Naohisa; Higuchi, M.; Kusuyama, Taro; Iso, Yoshitaka; Kobayashi, Naohiko; Yokoyama, Sin-Ichiro; Fukuda, Noboru; Saitoh, Hisao; Akazawa, Kohei; Aizawa, Yoshifusa

doi:10.1620/tjem.218.93

Cited by 33 publications

(23 citation statements)

References 27 publications

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“…It has been shown, in the rat model of myocardial infarction (MI), that Hamp mRNA and HAMP protein are elevated in the ischemic myocardium during the acute phase (Simonis et al, 2010). In humans, circulating HAMP was shown to be elevated in the serum within 4 hr of MI, although the tissue source of this hepcidin was not identified (Suzuki et al, 2009). In addition, decreased cardiac HAMP expression has been reported in a transgenic mouse model of dilated cardiomyopathy, where the phenotype was ameliorated following transgenic overexpression of cardiac hepcidin (Zhang et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Lakhal‐Littleton

Wolna

Chung

et al. 2016

eLife

149

192

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Hepcidin is the master regulator of systemic iron homeostasis. Derived primarily from the liver, it inhibits the iron exporter ferroportin in the gut and spleen, the sites of iron absorption and recycling respectively. Recently, we demonstrated that ferroportin is also found in cardiomyocytes, and that its cardiac-specific deletion leads to fatal cardiac iron overload. Hepcidin is also expressed in cardiomyocytes, where its function remains unknown. To define the function of cardiomyocyte hepcidin, we generated mice with cardiomyocyte-specific deletion of hepcidin, or knock-in of hepcidin-resistant ferroportin. We find that while both models maintain normal systemic iron homeostasis, they nonetheless develop fatal contractile and metabolic dysfunction as a consequence of cardiomyocyte iron deficiency. These findings are the first demonstration of a cell-autonomous role for hepcidin in iron homeostasis. They raise the possibility that such function may also be important in other tissues that express both hepcidin and ferroportin, such as the kidney and the brain.DOI: http://dx.doi.org/10.7554/eLife.19804.001

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Section: Discussionmentioning

confidence: 99%

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Lakhal‐Littleton

Wolna

Chung

et al. 2016

eLife

149

192

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“…A study on acute cardiac ischemia showed a transient increase in serum hepcidin-20 concentrations for the majority of patients studied, whereas hepcidin-25 remained increased 7 days after the incident. The authors concluded that hepcidin-20, rather than hepcidin-25, may be helpful for the diagnosis of acute myocardial infarction (14 ).…”

Section: Disorders Associated With Hepcidin Excessmentioning

confidence: 99%

“…Interestingly, these smaller hepcidin isoforms occur only in serum of patients with diseases that are associated with increased concentrations of hepcidin-25, such as acute myocardial infarction (AMI), 4 sepsis, anemia of chronic disease (ACD), metabolic syndrome, and chronic kidney disease (CKD) ( Fig. 2) (12)(13)(14)(15)(16)(17). In vivo studies in mice have demonstrated that only full-length 25 amino acid hepcidin induces significant hypoferremia when injected intraperitoneally (18 ).…”

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confidence: 99%

Hepcidin in Human Iron Disorders: Diagnostic Implications

et al. 2011

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BACKGROUND:The peptide hormone hepcidin plays a central role in regulating dietary iron absorption and body iron distribution. Many human diseases are associated with alterations in hepcidin concentrations. The measurement of hepcidin in biological fluids is therefore a promising tool in the diagnosis and management of medical conditions in which iron metabolism is affected.CONTENT: We describe hepcidin structure, kinetics, function, and regulation. We moreover explore the therapeutic potential for modulating hepcidin expression and the diagnostic potential for hepcidin measurements in clinical practice.

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“…Oğuz et al (7) reported that hepcidin levels did not increased in stable patients who had previously experienced atherosclerotic event as a marker of chronic inflammation. Conversely, Suzuki et al (5) showed that the serum hepcidin level was transiently elevated in response to acute cardiac ischemia in patients with AMI. In an experimental study, Isoda et al (6) demonstrated that hepcidin was strongly induced in cardiomyocytes under myocarditis and myocardial infarction.…”

Section: Discussionmentioning

confidence: 98%

Assessment of serum hepcidin levels in patients with non-ST elevation myocardial infarction

Altun¹,

Altun²,

Acar³

et al. 2014

Anadolu Kardiyol Derg

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Objective: Hepcidin is an acute-phase reactant produced in the liver displaying intrinsic antimicrobial activity. There are few studies about hepcidin considered to be acute and chronic inflammatory marker in acute coronary syndromes patients. We investigated in our study whether the level of hepcidin has increased in the acute phase of non-ST elevation myocardial infarction patients (NSTEMI) known as acute inflammatory aggravation of chronic atherosclerotic process. Methods: Seventy patients with NSTEMI and twenty healthy people were recruited as controls in this observational cross-sectional study. Serum hepcidin levels were determined by ELISA, and troponin levels were measured by standard laboratory methods. Levels of hepcidin and troponin were measured at admission and 6 hours later. Mean values of continuous variables were compared between groups using the Student t-test or Mann-Whitney U test, according to whether normally distributed or not, as tested by the Kolmogorov-Smirnov test. Serum troponin and hepcidin levels measured at admission and after 6 th hours were compared using paired t-test. Results: Hepcidin level was similar between NSTEMI and controls at admission (24.55±32.13, 23.67±33.62 ng/mL, p>0.05, respectively). Also, serum hepcidin levels did not change significantly from baseline in blood samples taken after 6 hour from admission in NSTEMI patients (24.55±32.13 ng/mL, 29.75±31.48 ng/mL, p=0.62, respectively). However, serum troponin levels were increased significantly compared to baseline (0.29±3.56, 2.92±7.2 ng/mL, p<0.01). Conclusion: Our findings suggest that hepcidin could not be use as a marker of myocardial necrosis in acute phase such as troponin in patients with NSTEMI. (Anadolu Kardiyol Derg 2014; 14: 515-8)

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Serum Hepcidin-20 is Elevated during the Acute Phase of Myocardial Infarction

Cited by 33 publications

References 27 publications

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

An essential cell-autonomous role for hepcidin in cardiac iron homeostasis

Hepcidin in Human Iron Disorders: Diagnostic Implications

Assessment of serum hepcidin levels in patients with non-ST elevation myocardial infarction

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