ArticleJournal of lipid research2010
Participation of ATP7A in macrophage mediated oxidation of LDL.
Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026Review
- Copper homeostasis in macrophages: regulatory mechanisms and immunological implications.Frontiers in chemistry · 2026Review
- The molecular mechanisms of cuproptosis and its relevance to atherosclerosis.Biomolecules & biomedicine · 2025Review
- A New Insight on Atherosclerosis Mechanism and Lipid-Lowering Drugs.Reviews in cardiovascular medicine · 2025Review
- Copper ions: The invisible killer of cardiovascular disease (Review).Molecular medicine reports · 2024Review
- Emerging insights into cuproptosis and copper metabolism: implications for age-related diseases and potential therapeutic strategies.Frontiers in aging neuroscience · 2024Review
- Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies.Cell death & disease · 2023Review
- Adipocyte-specific disruption of ATPase copper transporting α in mice accelerates lipoatrophy.Diabetologia · 2019Article
- Copper Transporter ATP7A (Copper-Transporting P-Type ATPase/Menkes ATPase) Limits Vascular Inflammation and Aortic Aneurysm Development: Role of MicroRNA-125b.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Copper transporters and copper chaperones: roles in cardiovascular physiology and disease.American journal of physiology. Cell physiology · 2018Review
- Bone marrow from blotchy mice is dispensable to regulate blood copper and aortic pathologies but required for inflammatory mediator production in LDLR-deficient mice during chronic angiotensin II infusion.Annals of vascular surgery · 2015Article
- Pathogenic adaptations to host-derived antibacterial copper.Frontiers in cellular and infection microbiology · 2014Review
- Human macrophage ATP7A is localized in the trans-Golgi apparatus, controls intracellular copper levels, and mediates macrophage responses to dermal wounds.Inflammation · 2012Article
- Conditional knockout of the Menkes disease copper transporter demonstrates its critical role in embryogenesis.PloS one · 2012Article
- Advances in the understanding of mammalian copper transporters.Advances in nutrition (Bethesda, Md.) · 2011Review
- Human copper homeostasis: a network of interconnected pathways.Current opinion in chemical biology · 2010Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
ATP7A primarily functions to egress copper from cells, thereby supplying this cofactor to secreted copper-accepting enzymes. This ATPase has attracted significant attention since the discovery of its mutation leading to human Menkes disease and the demonstration of its distribution in various tissues. Recently, we reported that ATP7A is expressed in the human vasculature. In the present study, we investigated the cellular expression of ATP7A in atherosclerotic lesions of LDL receptor (-/-) mice. Subsequently, we examined the role of ATP7A in regulating the oxidation of LDL in a macrophage cell model. We observed that ATP7A is expressed in atherosclerotic murine aorta and colocalizes with macrophages. To investigate the function of ATP7A, we downregulated ATP7A expression in THP-1 derived macrophages using small interfering RNA (siRNA). ATP7A downregulation attenuated cell-mediated oxidation of LDL. Moreover, downregulation of ATP7A resulted in decreased expression and enzymatic activity of cytosolic phospholipase A(2) alpha (cPLA(2)alpha), a key intracellular enzyme involved in cell-mediated LDL oxidation. In addition, cPLA(2)alpha promoter activity was decreased after downregulation of ATP7A, suggesting that ATP7A transcriptionally regulates cPLA(2)alpha expression. Finally, cPLA(2)alpha overexpression increased LDL oxidation, which was blocked by coadministration of ATP7A siRNA oligonucleotides. These findings suggest a novel mechanism linking ATP7A to cPLA(2)alpha and LDL oxidation, suggesting that this copper transporter could play a previously unrecognized role in the pathogenesis of atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.