Is copper a new target to counteract the progression of chronic diseases?

Balsano, Clara; Porcu, Cristiana; Sideri, Silvia

doi:10.1039/c8mt00219c

Cited by 51 publications

(35 citation statements)

References 94 publications

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“…Copper levels are tightly regulated, and its imbalance can have implications on the development and progression of both chronic and inflammatory diseases (including metabolic, cardiovascular, and neurodegenerative diseases). It can also predispose to malignant processes [68]. A deficit in copper levels can cause impaired levels of energy, abnormal glucose and cholesterol metabolism, increased oxidative damage, and altered function and structure of circulating blood and immune cells [69,70].…”

Section: Coppermentioning

confidence: 99%

The Role of Zinc and Copper in Gynecological Malignancies

Michalczyk

Cymbaluk‐Płoska

2020

Nutrients

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Zinc (Zn) and copper (Cu) are essential microelements, which take part in cellular metabolism, feature in enzymatic systems, and regulate enzyme activity. Homeostasis of these micronutrients is tightly regulated by multiple compensatory mechanisms that balance their concentrations including transporters, importers, and metallothioneins. An altered intake of only one of these trace elements may cause an imbalance in their levels and result in their competition for absorption. Relatively low levels of zinc and increased levels of copper may result in an increased level of oxidative stress and impair the antioxidant properties of multiple enzymes. Altered levels of trace elements were discovered in various pathologies including immunological, degenerative, and inflammatory diseases. Moreover, due to the role of Zn and Cu in oxidative stress and chronic inflammation, they were found to influence cancerogenesis. We review the roles of zinc and copper and their mechanisms in tumor growth, metastasis potential, microenvironment remodeling, and drug resistance. We highlight their role as potential biomarkers for cancer diagnosis, treatment, and prognosis, concentrating on their impact on gynecological malignancies.

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Section: Coppermentioning

confidence: 99%

The Role of Zinc and Copper in Gynecological Malignancies

Michalczyk

Cymbaluk‐Płoska

2020

Nutrients

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“…Copper (Cu) participates in the production of energy in the mitochondria and functions as a cofactor to superoxide dismutase (SOD) found in the cytosol and intracellular space. Over the years, copper imbalances have been linked to chronic inflammatory diseases [179].…”

Section: Influence Of Antioxidants In Diabetic Retinopathymentioning

confidence: 99%

Oxidative Stress as the Main Target in Diabetic Retinopathy Pathophysiology

Olvera-Montaño

Alberto

Navarro-Partida

et al. 2019

Journal of Diabetes Research

120

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Diabetic retinopathy (DR) is one of the most common complications of diabetes mellitus (DM) causing vision impairment even at young ages. There are numerous mechanisms involved in its development such as inflammation and cellular degeneration leading to endothelial and neural damage. These mechanisms are interlinked thus worsening the diabetic retinopathy outcome. In this review, we propose oxidative stress as the focus point of this complication onset.

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“…The presence of a proinflammatory milieu in the airway is an important characteristic of a variety of chronic pulmonary diseases, such as COPD and asthma, and inflammation plays critical roles in the development of these diseases 15–18 . Although some studies have suggested that inflammatory responses influence copper homeostasis in cells, 19–22 the definitive relationship between inflammation and copper homeostasis remains unclear. Environmental copper, which typically exists in the cupric state, must be firstly reduced to a cuprous state by membrane‐bound metalloreductases 20,23 .…”

Section: Introductionmentioning

confidence: 99%

Inflammation accelerates copper‐mediated cytotoxicity through induction of six‐transmembrane epithelial antigens of prostate 4 expression

Jiang

Xue

et al. 2021

Immunol. Cell Biol.

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Copper is an essential trace metal, but imbalance in copper homeostasis can induce oxidative damage. Inflammation is a fundamental element of various pulmonary diseases. Although a positive relationship between copper and chronic pulmonary diseases has been reported, the underlying reasons are still not clear. The copper level in the sputum of patients with various pulmonary diseases was measured. An inflammatory model was established to evaluate the impact of inflammation on copper uptake in the lung. We found that the level of sputum copper was increased in patients with various pulmonary diseases, especially chronic obstructive pulmonary disease and asthma. Then, we confirmed that mice with pulmonary inflammation were susceptible to copper‐mediated oxidative damage because of copper overload in lung tissue. Further investigation demonstrated that interleukin (IL)‐17 and tumor necrosis factor (TNF)‐α exerted synergistic effects in airway epithelial cells by upregulating the expression of six‐transmembrane epithelial antigens of prostate 4 (STEAP4), a metalloreductase that reduces extracellular copper ions from the cupric state to the cuprous state and facilitates copper uptake. Inhibition of STEAP4 decreased the copper uptake of cells and inhibited copper‐mediated oxidative damage. Moreover, we demonstrated that the upregulation of STEAP4 by IL‐17 and TNF‐α was largely dependent on TNF receptor‐associated factor 4 (TRAF4). Traf4−/− mice were resistant to copper‐mediated oxidative damage. Our data suggest a novel IL‐17/TNF‐α–TRAF4–STEAP4 axis that regulates copper homeostasis.

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Is copper a new target to counteract the progression of chronic diseases?

Abstract: In this review, we highlight the importance of a Cu imbalance in the pathogenesis of several chronic inflammatory diseases.

Cited by 51 publications

References 94 publications

The Role of Zinc and Copper in Gynecological Malignancies

The Role of Zinc and Copper in Gynecological Malignancies

Oxidative Stress as the Main Target in Diabetic Retinopathy Pathophysiology

Inflammation accelerates copper‐mediated cytotoxicity through induction of six‐transmembrane epithelial antigens of prostate 4 expression

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