The possible association of mitochondrial fusion and fission in copper deficiency-induced oxidative damage and mitochondrial dysfunction of the heart

Wei, Tianlong; Wang, Qinxu; Chen, Tao; Zhou, Zhiyuan; Li, Shuangfei; Li, Zhengfeng; Zhang, Dayong

doi:10.1016/j.jtemb.2024.127483

Journal of Trace Elements in Medicine and Biology

2024

DOI: 10.1016/j.jtemb.2024.127483

|View full text |Cite

The possible association of mitochondrial fusion and fission in copper deficiency-induced oxidative damage and mitochondrial dysfunction of the heart

Tianlong Wei,

Qinxu Wang,

Tao Chen

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

2025

Publication Types

Select...

Article3

Relationship

Self Cite0

Independent3

Authors

Journals

Cited by 3 publications

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Synthesis and characterization of biopolymer-based copper carbonate nanoparticles

Blinov,

Yasnaya,

Gvozdenko

et al. 2025

Materials Today Communications

View full text Add to dashboard Cite

Synthesis and characterization of biopolymer-based copper carbonate nanoparticles

Blinov,

Yasnaya,

Gvozdenko

et al. 2025

Materials Today Communications

View full text Add to dashboard Cite

Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets

Lv,

Zhao,

Song

et al. 2024

IJMS

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is a leading cause of death globally, with atherosclerosis (AS) playing a central role in its pathogenesis as a chronic inflammatory condition. Copper, an essential trace element in the human body, participates in various biological processes and plays a significant role in the cardiovascular system. Maintaining normal copper homeostasis is crucial for cardiovascular health, and dysregulation of copper balance is closely associated with the development of CVD. When copper homeostasis is disrupted, it can induce cell death, which has been proposed to be a novel form of “cuproptosis”, distinct from traditional programmed cell death. This new form of cell death is closely linked to the occurrence and progression of AS. This article elaborately describes the physiological mechanisms of copper homeostasis and explores its interactions with signaling pathways related to AS. Additionally, we focus on the process and mechanism of cell death induced by imbalances in copper homeostasis and summarize the relationship between copper homeostasis-related genes and AS. We also emphasize potential therapeutic approaches, such as copper balance regulators and nanotechnology interventions, to adjust copper levels in the body, providing new ideas and strategies for the prevention and treatment of CVD.

show abstract

Impacts of Copper Deficiency on Oxidative Stress and Immune Function in Mouse Spleen

Li,

Zeng,

Yang

et al. 2024

Nutrients

View full text Add to dashboard Cite

Introduction: Copper is an essential trace element crucial for enzyme synthesis and metabolism. Adequate copper levels are beneficial for maintaining the normal immune function of the spleen. Copper deficiency disrupts the metabolic processes within the spleen and impairs its immune function. This research examines the impact of copper deficiency on the spleen and the potential recovery following copper supplementation. Methods: Weaned mice underwent a 4-week copper-deficient diet, succeeded by 1-week of copper repletion via intraperitoneal copper sulfate injection. Histological examination was used to assess pathological changes in the spleen. Biochemical assays were performed to measure oxidative stress levels in the spleen. ELISA, qPCR, and Western blot were employed to examine alterations in inflammatory markers, immune indicators, and oxidative regulatory factors across various levels. Results: Copper deficiency caused histological damage to the spleen, altered the expression of oxidative stress regulatory pathways (Nrf2, Keap1, and HO-1), and affected the expression of key inflammatory enzymes (iNOS, COX2) and transcription factor NF-κB, leading to oxidative damage. This was reflected by decreased levels of SOD, GSH, and T-AOC, along with increased levels of CAT and MDA. The levels of inflammatory cytokines IL-1β, TNF-α, IL-6, and IL-8 were notably increased. Copper supplementation significantly improved these changes. Conclusions: Copper deficiency leads to spleen tissue damage in mice, affecting the Nrf2 regulatory pathway and inducing oxidative damage. Subsequent copper supplementation with copper sulfate effectively ameliorates the damage caused by copper deficiency.

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

The possible association of mitochondrial fusion and fission in copper deficiency-induced oxidative damage and mitochondrial dysfunction of the heart

Cited by 3 publications

References 42 publications

Synthesis and characterization of biopolymer-based copper carbonate nanoparticles

Synthesis and characterization of biopolymer-based copper carbonate nanoparticles

Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets

Impacts of Copper Deficiency on Oxidative Stress and Immune Function in Mouse Spleen

Contact Info

Product

Resources

About