Studies have shown an association between cardiovascular disease and abnormal copper metabolism. Cuproptosis is caused by the accumulation of copper in vivo, and is a newly identified form of cell death. It regulates cardiovascular diseases by affecting vascular endothelial function and myocardial energy metabolism through pathways such as oxidative stress, mitochondrial function, and gene expression. The treatment of copper accumulation in traditional Chinese medicine primarily involves heat-clearing and detoxification therapy, supplemented with diuretic therapy. In contrast, Western medicine mainly uses copper chelators. Flavonoids are common active ingredients used in the treatment of copper metabolism-related and cardiovascular diseases. In this article, we reviewed the relationship between copper metabolism, cuproptosis, and cardiovascular disease, providing novel strategies for preventing and treating cardiovascular disease; our ultimate aim is to encourage inspiration and contemplation among readers.
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http://dx.doi.org/10.1097/FJC.0000000000001653 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Chemistry, University of California, Berkeley, CA 94720.
Copper is an essential nutrient for sustaining vital cellular processes spanning respiration, metabolism, and proliferation. However, loss of copper homeostasis, particularly misregulation of loosely bound copper ions which are defined as the labile copper pool, occurs in major diseases such as cancer, where tumor growth and metastasis have a heightened requirement for this metal. To help decipher the role of copper in the etiology of cancer, we report a histochemical activity-based sensing approach that enables systematic, high-throughput profiling of labile copper status across many cell lines in parallel.
View Article and Find Full Text PDFRSC Adv
January 2025
Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences Tehran Iran
Due to the presence of the pyridyl directing group, -aryl-2-aminopyridines can quickly form stable complexes with metals, leading to cyclization and functionalization reactions. A large number of N-heterocycles and nitrogen-based molecules can be easily constructed this direct and atom-economical cross-coupling strategy. In this review, we have highlighted the transformations of -aryl-2-aminopyridines in the presence of various transition metal catalysts, such as palladium, rhodium, iridium, ruthenium, cobalt and copper.
View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Department of Pharmacy The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation.
View Article and Find Full Text PDFMedicine (Baltimore)
November 2024
First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, China.
This study investigates levels of cuproptosis markers in Wilson disease (WD) and their role in the occurrence and development of WD. We retrospectively collected clinical data from 76 patients with Leipzig score ≥ 4 hospitalized in the First Affiliated Hospital of Anhui University of Chinese Medicine from January 2023 to September 2023. The participants were given copper chelators (sodium dimercaptosulphonate (20 mg·kg-1), 4 courses of treatment, 32 days).
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Health Sciences Institute of China Medical University, Shenyang 110122, China. Electronic address:
Recently study has found a new form of copper-dependent death called cuproptosis, which differs from apoptosis, ferroptosis, and necrosis. The main process of cuproptosis is copper directly combined with lipid-acetylated proteins in the TCA cycle of mitochondrial response, leading to the aggregation of lipid-acetylated proteins and the loss of Fe-S cluster proteins, resulting in mitochondrial dysfunction, and eventually causing cell death. Previous studies demonstrated that an imbalance in copper homeostasis exacerbates the pathological progression of Alzheimer's disease (AD) through the induction of oxidative stress, inflammatory response, and the accumulation of Aβ deposition and tau protein hyperphosphorylation.
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