Hepcidin and iron metabolism disorders in patients with chronic kidney disease

Jelić, Marija; Cvetković, Tatjana; Đorđević, Vidojko; Damnjanović, Goran; Vlahović, Predrag; Kocić, Gordana; Đinđić, Nataša; Jovović, Biljana; Antić, Ana

doi:10.2298/vsp1304368j

Cited by 8 publications

(10 citation statements)

References 36 publications

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“…Hepcidin inhibits iron egress out of cells through binding and inducing degradation of its receptor ferroportin. Ferroportin, the only known mammalian iron exporter is mainly expressed in epithelial cells in duodenum and macrophages (Jelic et al, 2013;Pinnix et al, 2010). Suppression of hepcidin expression or hepcidin deficiency would cause enhanced iron egress out of macrophages, leading to iron overload in various organs, associated with neoplasia, arthropathy and neurodegenerative diseases (Jelic et al, 2013;Pinnix et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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Osteoporosis is one of the leading disorders among aged people. Bone loss results from a number of physiological alterations, such as estrogen decline and aging. Meanwhile, iron overload has been recognized as a risk factor for bone loss. Systemic iron homeostasis is fundamentally governed by the hepcidin-ferroportin regulatory axis, where hepcidin is the key regulator. Hepcidin deficiency could induce a few disorders, of which iron overload is the most representative phenotype. However, there was little investigation of the effects of hepcidin deficiency on bone metabolism. To this end, hepcidin-deficient (Hamp1 −/− ) mice were employed to address this issue. Our results revealed that significant iron overload was induced in Hamp1 −/− mice. Importantly, significant decreases of maximal loading and maximal bending stress were found in Hamp1 −/− mice relative to wildtype (WT) mice.Moreover, the levels of the C-telopeptide of type I collagen (CTX-1) increased in Hamp1 −/− mice. Therefore, hepcidin deficiency resulted in a marked reduction of bone load-bearing capacity likely through enhancing bone resorption, suggesting a direct correlation between hepcidin deficiency and bone loss. Targeting hepcidin or the pathway it modulates may thus represent a therapeutic for osteopenia or osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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“…This is began with DM nephropathy that if continued and uncontrolled will cause chronic kidney failure. 9 Blood Urea Nitogen (BUN) and creatinine levels pre-HD were found to be 49.49±15.6 mg/dL and 10.77±2.7 mg/dL, respectively. The mean of creatinine level in this study was higher than a previous study by Krishnamurthy 7 which showed a creatinine level of 7.22±2.22 mg/dL.…”

Section: Sexmentioning

confidence: 99%

“…This number was lower compared with the results of a study conducted by Jeli in Serbia (88%). 9 Hypertension is one of risk factor for chronic renal disease, this maybe because a severe and uncontrolled hypertension will cause changes in arterioles vessel walls (arteriol fibrinoid sclerosis) and will impair the renal function, on the other side, hypertension may also be an impact from chronic renal disease (renal hypertension). 9 There was a total of 28.9% of subjects who had risk factor for diabetes mellitus.…”

Section: Sexmentioning

confidence: 99%

Balance of Proinflammatory and Anti Inflammatory Markers in Routine Hemodialyzed Patients (A Study of End-Stage Renal Failure Patients at the Dr. Sardjito Hospital Yogyakarta)

Puspitawati

Purwanto

Suromo

2018

Indonesian J. Clin. Pathol. Med. Lab.

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Patients with End-Stage Renal Disease (ESRD) tend to have immune imbalance triggered by uremia and Hemodialysis (HD) procedures. Contact between dialysis membrane and blood will cause bio-incompatibility reactions inducing complement activation and production of Reactive Oxygen Species (ROS) as well as proinflammatory cytokines and acute phase protein such as C-Reactive Protein (CRP). Those immune response imbalances will lead to an immunocompromised condition. The objective of this study was to prove the correlation between inflammatory markers (IL-1β, IL-6 and C-reactive proteins) and its anti-inflammatory marker (IL-10) in routine hemodialyzed patients. This is a cross-sectional observational study involving 90 subjects conducted at the Hemodialysis Installation of the Dr. Sardjito Hospital. The inclusion criteria of this study were patients who underwent routine HD procedures, aged between 18 and 65 years-old, having leukocytes count and albumin level within normal limit. The exclusion criteria of this study were patients with Acute Coronary Syndrome (ACS) and malignancies. Levels of IL-1β, IL-6 and IL-10 were measured using Enzyme-Linked Immunosorbent Assay (ELISA), while CRP was measured using highly-sensitive CRP immunoturbidimetry. Statistical analysis was performed by Spearman test. This study results showed correlations between IL-1βand IL-10 (p=0.001, r=0.302), IL-6 and IL-10 (p=0.001, r=0.418) and correlation between CRP and IL-10 (p=0.005, r=0.295). There were also correlations between IL-1β and IL-6 (p=0.029, r=0.232), IL-6 and CRP (p=0.001, r=0.534), but no correlation was found between IL- 1β and CRP (p=0.431, r=0.073). All factors that trigger the secretion of proinflammatory cytokines will trigger the release of anti-inflammatory cytokines, the consequences of anti-inflammatory cytokine secretion will happen minutes after the release of inflammatory cytokines. This study showed that there were correlations between proinflammatory and anti-inflammatory cytokines. Further studies of polymorphism-related cytokines secretion are warranted.

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“…Liver is the central organ governing systemic iron homeostasis, where hepcidin is primarily secreted by hepatocytes and regulates iron flux by interacting with its receptor ferroportin, which is associated with the internalization and degradation of ferroportin, thereby reducing iron egress from macrophages and iron absorption from the small intestine (14)(15)(16). Iron, an essential element, is important for a variety of biological processes (17,18).…”

Section: Introductionmentioning

confidence: 99%

“…Systemic iron homeostasis is deliberately modulated by the hepcidin-ferroportin regulatory axis (14,(19)(20)(21). Ferroportin is the only known mammalian iron exporter, mainly expressed in epithelial cells in duodenum and macrophages, and is critical for controlling iron egress (15,16). Through the hepcidin-ferroportin axis, downregulated hepatic hepcidin increases the serum iron level by promoting iron absorption from enterocytes in duodenum and iron release from macrophages (22).…”

Section: Introductionmentioning

confidence: 99%

Sublethal exposure of organophosphate pesticide chlorpyrifos alters cellular iron metabolism in hepatocytes and macrophages

Sun

Zhang

Guo

et al. 2014

International Journal of Molecular Medicine

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Chlorpyrifos (CPF) is commonly used for agricultural and domestic applications, and its contamination is widely detected in environmental media, and in a broad spectrum of field crops, fruits and vegetables. CPF exposure causes many adverse effects on human health including hepatoxicity, neurotoxicity and endocrine disruption. However, few studies have been conducted thus far to investigate the potential influence of CPF exposure on iron metabolism at concentrations that do not trigger significant cell death. Iron metabolism is concertedly governed by the hepcidin-ferroportin axis, where hepcidin is the central hormone involved in the regulation of iron absorption and release, while ferroportin is the only known iron exporter that functions by iron egress from cells. In the present study, we demonstrated that CPF treatment at a non-toxic concentration greatly enhanced ferroportin gene transcription in human macrophage THP-1 cells. CPF significantly inhibited hepcidin expression in human hepatocyte HepG2 cells. As a result, the intracellular labile iron pool (LIP) was largely reduced in THP-1 and HepG2 cells. The combined data of this study identified a novel finding of CPF that disrupts iron homeostasis by altering ferroportin and hepcidin expression. These findings would be useful in understanding the biological effects of CPF exposure, especially under relatively low and non-toxic doses.

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Hepcidin and iron metabolism disorders in patients with chronic kidney disease

Abstract: Hepcidin may serve as a marker for better diagnosing and monitoring anemia and iron metabolism disorders in CKD.

Cited by 8 publications

References 36 publications

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Balance of Proinflammatory and Anti Inflammatory Markers in Routine Hemodialyzed Patients (A Study of End-Stage Renal Failure Patients at the Dr. Sardjito Hospital Yogyakarta)

Sublethal exposure of organophosphate pesticide chlorpyrifos alters cellular iron metabolism in hepatocytes and macrophages

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