Role of cuproptosis in understanding diseases

Abstract

Cell death is involved in a wide range of physiological and pathological processes. Recently, the term “cuproptosis” was coined to describe a novel type of cell death. This type of cell death, characterized by copper accumulation and proteotoxic stress, is a copper-dependent manner of death. Despite the progress achieved toward a better understanding of cuproptosis, mechanisms and related signaling pathways in physiology and pathology across various diseases remain to be proved. This mini review summarizes current research on cuproptosis and diseases, providing insights into prospective clinical therapies via targeting cuproptosis.

An effective prognostic model in colon adenocarcinoma composed of cuproptosis-related epigenetic regulators

“…Copper levels in cancer cells are typically higher than in normal cells, which may give them an advantage during angiogenesis, invasion, and metastasis, but also result in enhanced vulnerability to cuproptosis ( Xie et al, 2023 ). Therefore, cuproptosis could serve as a viable therapeutic target in the fight against cancer, including COAD ( Cao et al, 2023 ).…”

Cuproptosis: Unraveling the Mechanisms of Copper-Induced Cell Death and Its Implication in Cancer Therapy

“…Disruption of copper homeostasis, and oxidative stress FDX1 [23] DLAT [23] DBT [23] GCSH [23] DLST [23] LIAS [23] CTR1 [23] ATP7A/ATP7B [24] MT [24] GSH [24] PDH [25] PDHA1 [25] PDHB [25] KDH [26] SLC31A1 [27,28] LIPT1 [29] Neurological diseases (e.g., Menkes and Wilson) [26]. Cancer (e.g., elevated serum copper levels in oral, gallbladder, liver, breast, esophageal, pancreatic, bladder, renal, prostatic, thyroid, cervical, and lung; decreased serum copper levels in endometrial and colorectal) [10,31]. While cuproptosis shares commonalities in proteins and lipids with other forms of cell death like apoptosis [19], ferroptosis [20], and pyroptosis [21], it also exhibits distinct molecular mechanisms that distinguish it as a distinct form of cell death [22].…”

“…Disruption of copper homeostasis, and oxidative stress FDX1 [23] DLAT [23] DBT [23] GCSH [23] DLST [23] LIAS [23] CTR1 [23] ATP7A/ATP7B [24] MT [24] GSH [24] PDH [25] PDHA1 [25] PDHB [25] KDH [26] SLC31A1 [27,28] LIPT1 [29] DLD [30] Neurological diseases (e.g., Menkes and Wilson) [26]. Cancer (e.g., elevated serum copper levels in oral, gallbladder, liver, breast, esophageal, pancreatic, bladder, renal, prostatic, thyroid, cervical, and lung; decreased serum copper levels in endometrial and colorectal) [10,31]. Iron-dependent lipid peroxidation GPX4 [32,33] GSH [34] DMT1 [16] Ferritin [35,36] 15-Lox [17] Neurodegenerative diseases (e.g., Alzheimer's and Parkinson's) [37].…”

“…Copper-induced cell death, also known as copper toxicity or cuproptosis, describes the harmful effects that excessive copper levels induce on cellular processes [10]. Cuproptosis is a novel form of cell death, and the scientific community is in the process of unraveling its intricacies.…”

Role of extracellular vesicles associated with microRNAs and their interplay with cuproptosis in osteoporosis

“…The exosomal miRNA miR-21-5p, which is obtained from cisplatin-resistant SKOV3 ovarian cancer cells, enhances the glycolysis process and suppresses chemosensitivity of its progenitor SKOV3 cells through PDHA1 targeting [ 53 ]. PDHA1 is a cuproptosis-related gene (CRG), and it has an essential role in glucose metabolism, the TCA cycle, and mitochondrial oxidative phosphorylation [ 54 ]. PDHA1 inhibition might facilitate the proliferation of osteoblasts, while PDHA1 activation could affect macrophages and osteoblasts by inhibiting the release of inflammatory factors [ 8 ].…”