Copper homeostasis and copper-induced cell death： Novel targeting for intervention in the pathogenesis of vascular aging

Chen, Zhuoying; Li, Yuan-yuan; Liu, Xiangjie

doi:10.1016/j.biopha.2023.115839

Cited by 14 publications

(1 citation statement)

References 143 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…According to recent studies, Cu ions may slow the initiation and progression of atherosclerosis by encouraging the formation of vascular smooth muscle cells and blocking pathways associated with inflammation [ 150 , 151 ]. The serum Cu concentration is closely associated with atherosclerotic mortality [152] . However, the elemental copper content may vary with the severity of atherosclerotic lesions [153] .…”

Section: Molecular Cross-talk Between Ferroptosis and Other Types Of ...mentioning

confidence: 99%

Ferroptosis: a potential target for the treatment of atherosclerosis

Li,

Liu,

Xiong

et al. 2024

ABBS

View full text Add to dashboard Cite

Atherosclerosis (AS), the main contributor to acute cardiovascular events, such as myocardial infarction and ischemic stroke, is characterized by necrotic core formation and plaque instability induced by cell death. The mechanisms of cell death in AS have recently been identified and elucidated. Ferroptosis, a novel iron-dependent form of cell death, has been proven to participate in atherosclerotic progression by increasing endothelial reactive oxygen species (ROS) levels and lipid peroxidation. Furthermore, accumulated intracellular iron activates various signaling pathways or risk factors for AS, such as abnormal lipid metabolism, oxidative stress, and inflammation, which can eventually lead to the disordered function of macrophages, vascular smooth muscle cells, and vascular endothelial cells. However, the molecular pathways through which ferroptosis affects AS development and progression are not entirely understood. This review systematically summarizes the interactions between AS and ferroptosis and provides a feasible approach for inhibiting AS progression from the perspective of ferroptosis.

show abstract

Section: Molecular Cross-talk Between Ferroptosis and Other Types Of ...mentioning

confidence: 99%

Ferroptosis: a potential target for the treatment of atherosclerosis

Li,

Liu,

Xiong

et al. 2024

ABBS

View full text Add to dashboard Cite

show abstract

Copper homeostasis and cuproptosis in health and disease

Yang,

Wu,

Wang

et al. 2024

MedComm

View full text Add to dashboard Cite

Copper is a vital trace element in human physiology, essential for the synthesis of numerous crucial metabolic enzymes and facilitation of various biological processes. Regulation of copper levels within a narrow range is imperative for maintaining metabolic homeostasis. Numerous studies have demonstrated the significant roles of copper homeostasis and cuproptosis in health and disease pathogenesis. However, a comprehensive and up‐to‐date systematic review in this domain remains absent. This review aims to consolidate recent advancements in understanding the roles of cuproptosis and copper homeostasis in health and disease, focusing on the underlying mechanisms and potential therapeutic interventions. Dysregulation of copper homeostasis, manifesting as either copper excess or deficiency, is implicated in the etiology of various diseases. Cuproptosis, a recently identified form of cell death, is characterized by intracellular copper overload. This phenomenon mediates a diverse array of evolutionary processes in organisms, spanning from health to disease, and is implicated in genetic disorders, liver diseases, neurodegenerative disorders, and various cancers. This review provides a comprehensive summary of the pathogenic mechanisms underlying cuproptosis and copper homeostasis, along with associated targeted therapeutic agents. Furthermore, it explores future research directions with the potential to yield significant advancements in disease treatment, health management, and disease prevention.

show abstract

lncRNAs as prognostic markers and therapeutic targets in cuproptosis-mediated cancer

Bhat,

Afzal,

Moglad

et al. 2024

Clin Exp Med

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in various cellular processes, including cancer progression and stress response. Recent studies have demonstrated that copper accumulation induces a unique form of cell death known as cuproptosis, with lncRNAs playing a key role in regulating cuproptosis-associated pathways. These lncRNAs may trigger cell-specific responses to copper stress, presenting new opportunities as prognostic markers and therapeutic targets. This paper delves into the role of lncRNAs in cuproptosis-mediated cancer, underscoring their potential as biomarkers and targets for innovative therapeutic strategies. A thorough review of scientific literature was conducted, utilizing databases such as PubMed, Google Scholar, and ScienceDirect, with search terms like 'lncRNAs,' 'cuproptosis,' and 'cancer.' Studies were selected based on their relevance to lncRNA regulation of cuproptosis pathways and their implications for cancer prognosis and treatment. The review highlights the significant contribution of lncRNAs in regulating cuproptosis-related genes and pathways, impacting copper metabolism, mitochondrial stress responses, and apoptotic signaling. Specific lncRNAs are potential prognostic markers in breast, lung, liver, ovarian, pancreatic, and gastric cancers. The objective of this article is to explore the role of lncRNAs as potential prognostic markers and therapeutic targets in cancers mediated by cuproptosis.

show abstract

Copper homeostasis and copper-induced cell death： Novel targeting for intervention in the pathogenesis of vascular aging

Cited by 14 publications

References 143 publications

Ferroptosis: a potential target for the treatment of atherosclerosis

Ferroptosis: a potential target for the treatment of atherosclerosis

Copper homeostasis and cuproptosis in health and disease

lncRNAs as prognostic markers and therapeutic targets in cuproptosis-mediated cancer

Contact Info

Product

Resources

About