Hepcidin kao ključni regulator homeostaze željeza

undergraduate thesis

• Title (english): Hepcidin- central regulator of iron homeostasis
• Author: Barbara Toljanić
• Mentor: Nada Oršolić (mentor)
• Granter: University of Zagreb; Faculty of Science; (Department of Biology); Zagreb
• Defense date and country: 2021-09-15, Croatia
• Scientific / art field, discipline and subdiscipline: NATURAL SCIENCES; Biology

Abstract

Željezo je esencijalan element za gotovo sve žive organizme. Organizam održava homeostazu željeza, kontroliranjem apsorpcije željeza iz hrane enterocitima, recikliranjem putem makrofaga i skladištenjem u hepatocitima. Ove procese uglavnom kontrolira hepcidin. Hepcidin je peptid koji se sastoji od 25 aminokiselina i sintetizira se u jetri. Sinteza hepcidina je povećana ukoliko dolazi do nakupljanja željeza ili upale, a smanjuje se prilikom eritropoeze, anemije i hipoksije. Hepcidin inhibira istjecanje željeza iz stanice vežući se na feroportin, glavni eksporter željeza. Vezanjem za feroportin inducira njegovu internalizaciju i razgradnju u lizosomu. Smanjene koncentracije hepcidina mogu uzrokovati bolesti kao što su juvenilna hemokromatoza i anemiju s nakupljanjem željeza koja se javlja kod bolesnika s β-talasemijom. Višak hepcidina glavna je karakteristika anemije koja se javlja tijekom upale, anemije kroničnih bolesti i željezo refraktorne anemije uslijed nedostatka željeza. Velike količine slobodnog željeza mogu djelovati toksično jer kataliziraju stvaranje reaktivnih vrsta kisika, što dovodi do oksidativnog stresa i oštećenja tkiva. Pojava oksidativnog stresa može dovesti do nekih patoloških stanja vezanih uz reprodukciju i jetru te može biti uzrok neurodegenerativnih bolesti

Abstract (english)

Iron is an essential element for almost all living organisms. The body maintains iron homeostasis by controlling intestinal iron apsorption, recycling through macrophages, and storage in hepatocytes. These processes are mainly controlled by hepcidin. Hepcidin, 25-amino acid peptide, is synthesized in the liver. Hepcidin synthesis is greatly stimulated by iron overload or inflammation and decreased during erythropoiesis, anemia, and hypoxia. Hepcidin inhibits iron efflux from the cell by binding to ferroportin, the major exporter of iron. The hepcidin-ferroportin complex is internalized and degraded in the lysosome. Decreased hepcidin concentrations can cause diseases such as juvenile hemochromatosis and iron-loading anemia that occurs in patients with β-thalassemia. Excess hepcidin is a major feature of anemia that occurs during inflammation, anemia of chronic diseases, and iron-refractory iron deficiency anemia. Large amounts of free iron can be toxic because they catalyze the formation of reactive oxygen species, leading to oxidative stress and tissue damage. Oxidative stress have been linked to several pathological states related to reproduction and liver and can be the cause of neurodegenerative diseases.

• Keywords: Hepcidin; homeostaza željeza
• Language: croatian
• URN:NBN: urn:nbn:hr:217:461504
• Study programme: Title: Ecology; Study programme type: university; Study level: undergraduate; Academic / professional title: sveučilišni/a prvostupnik/prvostupnica (baccalaureus/baccalaurea) biologije (sveučilišni/a prvostupnik/prvostupnica (baccalaureus/baccalaurea) biologije)
• Type of resource: Text
• File origin: Born digital
• Access conditions: Open access
• Created on: 2021-09-16 11:03:14