We are analyzing https://link.springer.com/article/10.1007/s00424-020-02412-2.

Title:
The molecular mechanisms of copper metabolism and its roles in human diseases | Pflügers Archiv - European Journal of Physiology
Description:
Copper is an essential element in cells; it can act as either a recipient or a donor of electrons, participating in various reactions. However, an excess of copper ions in cells is detrimental as these copper ions can generate free radicals and increase oxidative stress. In multicellular organisms, copper metabolism involves uptake, distribution, sequestration, and excretion, at both the cellular and systemic levels. Mammalian enterocytes take in bioavailable copper ions from the diet in a Ctr1-dependent manner. After incorporation, cuprous ions are delivered to ATP7A, which pumps Cu+ from enterocytes into the blood. Copper ions arrive at the liver through the portal vein and are incorporated into hepatocytes by Ctr1. Then, Cu+ can be secreted into the bile or the blood via the Atox1/ATP7B/ceruloplasmin route. In the bloodstream, this micronutrient can reach peripheral tissues and is again incorporated by Ctr1. In peripheral tissue cells, cuprous ions are either sequestrated by molecules such as metallothioneins or targeted to utilization pathways by chaperons such as Atox1, Cox17, and CCS. Copper metabolism must be tightly controlled in order to achieve homeostasis and avoid disorders. A hereditary or acquired copper unbalance, including deficiency, overload, or misdistribution, may cause or aggravate certain diseases such as Menkes disease, Wilson disease, neurodegenerative diseases, anemia, metabolic syndrome, cardiovascular diseases, and cancer. A full understanding of copper metabolism and its roles in diseases underlies the identification of novel effective therapies for such diseases.
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Keywords {🔍}

pubmed, article, google, scholar, cas, copper, central, disease, biol, chem, role, med, metabolism, human, menkes, wilson, sci, transporter, cell, diseases, atpa, bush, superoxide, treatment, genet, mouse, chen, dismutase, alzheimers, acad, homeostasis, rev, proc, natl, nat, iron, kaler, cells, ions, wilsons, thiele, mol, clin, kim, model, zinc, essential, mechanisms, cox, metal,

Topics {✒️}

month download article/chapter copper-transporting p-type atpases copper-dependent stress-induced release egf-induced mapk signaling human cu-transporting atpases aaa atpase p97/vcp cytosolic metal-binding domain central nervous system hypoxia-induced pulmonary hypertension impaired stress-induced erythropoiesis menkes copper-transporting atpase copper-zinc chelator markedly full article pdf early copper-histidine treatment randomised placebo-controlled study copper-zinc superoxide dismutase fundamental research funds angiotensin ii-induced hypertension european economic area privacy choices/manage cookies speck-martins ce transition metal ions atox1/atp7b/ceruloplasmin route selective copper chelation copper uptake mediated review article bioavailable copper ions long-term measurement extracellular superoxide dismutase cooper gj lysosome-related organelles hypocupremia-related myeloneuropathy copper-dependent recycling article chen wilson disease-treatment perspectives human copper transporter ctr1-dependent manner uriu-hare jy de vivo dc central universities mammalian embryonic development metal-protein attenuation toxic milk mutation apical copper transporter la fontaine copper transporter atp7a toxic milk mouse ha-duong nt early fetal lethality concealed ubx domain

Questions {❓}

Bush AI, Curtain CC (2008) Twenty years of metallo-neurobiology: where to now?
Pierson H, Yang H, Lutsenko S (2019) Copper transport and disease: what can we learn from organoids?

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         description:Copper is an essential element in cells; it can act as either a recipient or a donor of electrons, participating in various reactions. However, an excess of copper ions in cells is detrimental as these copper ions can generate free radicals and increase oxidative stress. In multicellular organisms, copper metabolism involves uptake, distribution, sequestration, and excretion, at both the cellular and systemic levels. Mammalian enterocytes take in bioavailable copper ions from the diet in a Ctr1-dependent manner. After incorporation, cuprous ions are delivered to ATP7A, which pumps Cu+ from enterocytes into the blood. Copper ions arrive at the liver through the portal vein and are incorporated into hepatocytes by Ctr1. Then, Cu+ can be secreted into the bile or the blood via the Atox1/ATP7B/ceruloplasmin route. In the bloodstream, this micronutrient can reach peripheral tissues and is again incorporated by Ctr1. In peripheral tissue cells, cuprous ions are either sequestrated by molecules such as metallothioneins or targeted to utilization pathways by chaperons such as Atox1, Cox17, and CCS. Copper metabolism must be tightly controlled in order to achieve homeostasis and avoid disorders. A hereditary or acquired copper unbalance, including deficiency, overload, or misdistribution, may cause or aggravate certain diseases such as Menkes disease, Wilson disease, neurodegenerative diseases, anemia, metabolic syndrome, cardiovascular diseases, and cancer. A full understanding of copper metabolism and its roles in diseases underlies the identification of novel effective therapies for such diseases.
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