Identification of key genes for cuproptosis in carotid atherosclerosis DOI Creative Commons
Xize Wu, Jian Kang, Xue Pan

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Nov. 1, 2024

Atherosclerosis is a leading cause of cardiovascular disease worldwide, while carotid atherosclerosis (CAS) more likely to ischemic cerebrovascular events. Emerging evidence suggests that cuproptosis may be associated with an increased risk atherosclerotic disease. This study aims explore the potential mechanisms linking and CAS.

Language: Английский

Cardiovascular disease: Mitochondrial dynamics and mitophagy crosstalk mechanisms with novel programmed cell death and macrophage polarisation DOI Creative Commons
Dandan Liu,

Hewei Qin,

Yang Gao

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 206, P. 107258 - 107258

Published: June 21, 2024

Several cardiovascular illnesses are associated with aberrant activation of cellular pyroptosis, ferroptosis, necroptosis, cuproptosis, disulfidptosis and macrophage polarisation as hallmarks contributing to vascular damage abnormal cardiac function. Meanwhile, these three novel forms dysfunction closely related mitochondrial homeostasis. Mitochondria the main organelles that supply energy maintain Mitochondrial stability is maintained through a series regulatory pathways, such fission, fusion mitophagy. Studies have shown (e.g., impaired dynamics mitophagy) promotes ROS production, leading oxidative stress, which induces M1 phenotypic polarisation. Therefore, an in-depth knowledge dynamic regulation mitochondria during necessary understand disease development. This paper systematically summarises impact changes in mitophagy on regulating dysfunctions promote understanding pathogenesis diseases provide corresponding theoretical references for treating diseases.

Language: Английский

Citations

21

Copper homeostasis and cuproptosis in health and disease DOI Creative Commons

Yunuo Yang,

Jiaxuan Wu,

Lisheng Wang

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(10)

Published: Sept. 17, 2024

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

Language: Английский

Citations

7

Cuproptosis and copper deficiency in ischemic vascular injury and repair DOI
Jiayi Gu, Wei Huang,

Zheng Duanmu

et al.

APOPTOSIS, Journal Year: 2024, Volume and Issue: 29(7-8), P. 1007 - 1018

Published: April 22, 2024

Language: Английский

Citations

2

Identification of key genes for cuproptosis in carotid atherosclerosis DOI Creative Commons
Xize Wu, Jian Kang, Xue Pan

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Nov. 1, 2024

Atherosclerosis is a leading cause of cardiovascular disease worldwide, while carotid atherosclerosis (CAS) more likely to ischemic cerebrovascular events. Emerging evidence suggests that cuproptosis may be associated with an increased risk atherosclerotic disease. This study aims explore the potential mechanisms linking and CAS.

Language: Английский

Citations

0