Basics and principles of cellular and systemic iron homeostasis

Κατσαρού, Αλεξάνδρα; Pantopoulos, Kostas

doi:10.1016/j.mam.2020.100866

Cited by 123 publications

(101 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Under inflammatory conditions, increased serum interleukin-6 (IL-6) activates hepcidin expression via JAK/STAT3 signalling cascades, resulting in the promotion of hepcidin transcription [ 20 ]. Exercise and physical activities increase physiological demand and promote inflammation, which influences hepcidin expression and results in the development of acute anaemia of exercise (AAE).…”

Section: Introductionmentioning

confidence: 99%

Association of Serum Hepcidin Levels with Aerobic and Resistance Exercise: A Systematic Review

Larsuphrom

Latunde-Dada

2021

Nutrients

View full text Add to dashboard Cite

Background: Prevalence of iron deficiency is commonly reported among athletic population groups. It impairs physical performance due to insufficient oxygen delivery to target organs and low energy production. This is due to the high demand of exercise on oxygen delivery for systemic metabolism by the erythrocytes in the blood. Hepcidin, the key regulator of iron homeostasis, decreases to facilitate iron efflux into the circulation during enhanced erythropoiesis. However, acute anaemia of exercise is caused by increased hepcidin expression that is induced by stress and inflammatory signal. The study aimed to systematically review changes in serum hepcidin levels during resistance and aerobic exercise programmes. Methods: A systemic literature search from 2010 to April 2020 across seven databases comprised of Cochrane library, PubMed, Web of Science, Scopus, Embase, MEDLINE, and OpenGrey. The primary outcome was increased or decreased serum hepcidin from baseline after the exercise activity. Risks of bias were evaluated by using the National Institutes of Health (NIH) for quality assessment of before and after different exercise programmes. Results: Overall, twenty-three studies met the inclusion criteria. Out of the 23 studies, 16 studies reported significantly exercise-induced serum hepcidin elevation. Of the 17 studies that evaluated serum interleukin (IL)-6 levels, 14 studies showed significant exercise-induced serum IL-6 elevation. Changes in exercise-induced serum hepcidin and IL-6 levels were similar in both resistance and endurance exercise. Significant correlations were observed between post-exercise hepcidin and baseline ferritin levels (r = 0.69, p < 0.05) and between post-exercise hepcidin and post-exercise IL-6 (r = 0.625, p < 0.05). Conclusion: Resistance and endurance training showed significant increase in serum hepcidin and IL-6 levels in response to exercise. Baseline ferritin and post-exercise IL-6 elevation are key determining factors in the augmentation of hepcidin response to exercise.

show abstract

Section: Introductionmentioning

confidence: 99%

Association of Serum Hepcidin Levels with Aerobic and Resistance Exercise: A Systematic Review

Larsuphrom

Latunde-Dada

2021

Nutrients

View full text Add to dashboard Cite

show abstract

“…TF, a plasma iron carrier, expresses in liver and binds to plasma iron for transport. [ 31 ]…”

Section: Resultsmentioning

confidence: 99%

A Combined Model of Human iPSC‐Derived Liver Organoids and Hepatocytes Reveals Ferroptosis in DGUOK Mutant mtDNA Depletion Syndrome

Guo

Duan

et al. 2021

Advanced Science

View full text Add to dashboard Cite

Mitochondrial DNA depletion syndrome (MDS) is a group of severe inherited disorders caused by mutations in genes, such as deoxyribonucleoside kinase (DGUOK). A great majority of DGUOK mutant MDS patients develop iron overload progressing to severe liver failure. However, the pathological mechanisms connecting iron overload and hepatic damage remains uncovered. Here, two patients' skin fibroblasts are reprogrammed to induced pluripotent stem cells (iPSCs) and then corrected by CRISPR/Cas9. Patient-specific iPSCs and corrected iPSCs-derived high purity hepatocyte organoids (iHep-Orgs) and hepatocyte-like cells (iHep) are generated as cellular models for studying hepatic pathology. DGUOK mutant iHep and iHep-Orgs, but not control and corrected one, are more sensitive to iron overload-induced ferroptosis, which can be rescued by N-Acetylcysteine (NAC). Mechanically, this ferroptosis is a process mediated by nuclear receptor co-activator 4 (NCOA4)-dependent degradation of ferritin in lysosome and cellular labile iron release. This study reveals the underlying pathological mechanisms and the viable therapeutic strategies of this syndrome, and is the first pure iHep-Orgs model in hereditary liver diseases.

show abstract

“…Korábbi elképzelés szerint az ERFE járulékos sejtek nélkül, a STAT5 jelátviteli út aktivációjával direkt csökkenti a májsejtek hepcidinexpresszióját [3,38]. Újabb irodalmi adatok szerint a BMP fehérjék megkötése révén a SMAD jelátvitel blokkolása felelős a HAMP gén blokkolásáért [39]. Hatására az ún.…”

Section: Erythroferron (Erfe)unclassified

A vasanyagcsere szabályozása, hepcidinexpresszió fiziológiás és pathológiás körülmények között

Egyed

2021

Hematológia–Transzfuziológia

View full text Add to dashboard Cite

Összefoglaló. A humán szervezetnek az alapvető biokémiai reakcióihoz vasra és annak biztonságos használatára van szükség. Emberben vasexcretios út hiányában a vasanyagcsere sarkalatos pontja a duodenális absorptio, amelyet a májsejtek által termelt hormon, a hepcidin szabályoz. A hepcidin a ferroportin lisosomalis degradációját okozva blokkolja a vasnak a vérbe való belépését a duodenális enterocytából, a reticuloendothelialis rendszer (RES) macrophagokból és a májsejtekből. A reguláló hormon képzését a szervezet vaskészlete mellett az erythropoiesis, hypoxia és inflammatorikus folyamatok befolyásolják. A szabályozás kóros eltérései vashiány vagy vasterhelés útján súlyos betegségeket okozhatnak. A hepcidin képződését befolyásoló folyamatokat illetően ismereteink jelentősen gyarapodtak, közleményünk célja ezek bemutatása. Summary. The basic biochemical reactions of the human body require iron and its safe utilisation. In absence of an iron-excreation pathway in human, the pivotal point of iron metabolism is duodenal absorption, which is regulated by a hormone produced by liver cells, the hepcidin. Causing lisosomal degradation of ferroportin, hepcidin blocks the iron entry into the blood from duodenal enterocytes, reticuloendothelial system (RES) macrophages, and liver cells. In addition to the body’s iron stores, the production of the regulatory hormone is also affected by erythropoiesis, hypoxia and inflammatory processes. Abnormal regulation can lead to serious illness through iron deficiency or iron stress. Regarding the processes influencing the formation of hepcidin, our knowledge has significantly increased and the aim of our paper is to present them.

show abstract

Basics and principles of cellular and systemic iron homeostasis

Cited by 123 publications

References 73 publications

Association of Serum Hepcidin Levels with Aerobic and Resistance Exercise: A Systematic Review

Association of Serum Hepcidin Levels with Aerobic and Resistance Exercise: A Systematic Review

A Combined Model of Human iPSC‐Derived Liver Organoids and Hepatocytes Reveals Ferroptosis in DGUOK Mutant mtDNA Depletion Syndrome

A vasanyagcsere szabályozása, hepcidinexpresszió fiziológiás és pathológiás körülmények között

Contact Info

Product

Resources

About