The Cross-Communication of Cuproptosis and Regulated Cell Death in Human Pathophysiology DOI Creative Commons
Kuan‐Hao Tsui,

Jui‐Hu Hsiao,

Li‐Te Lin

et al.

International Journal of Biological Sciences, Journal Year: 2023, Volume and Issue: 20(1), P. 218 - 230

Published: Nov. 15, 2023

Copper (Cu) plays a crucial and diverse function in biological systems, acting as cofactor at numerous sites of enzymatic activity participating various physiological processes, including oxidative stress regulation, lipid metabolism, energy metabolism. Similar to other micronutrients, the body regulates Cu levels ensure homeostasis; any disruption homeostasis may result illnesses. Cuproptosis causes proteotoxic ultimately results cell death by binding ions lipid-acylated proteins during tricarboxylic acid cycle mitochondrial respiration. is not only involved regulatory (RCD), but also exogenous factors that induce cellular responses toxic outcomes. imbalances affect transmission several RCD messages. Therefore, this article presents thorough examination mechanisms Cu-induced well role complexes its pathophysiology.

Language: Английский

Copper metabolism in cell death and autophagy DOI Creative Commons
Qian‐Li Xue, Rui Kang, Daniel J. Klionsky

et al.

Autophagy, Journal Year: 2023, Volume and Issue: 19(8), P. 2175 - 2195

Published: April 14, 2023

Copper is an essential trace element in biological systems, maintaining the activity of enzymes and function transcription factors. However, at high concentrations, copper ions show increased toxicity by inducing regulated cell death, such as apoptosis, paraptosis, pyroptosis, ferroptosis, cuproptosis. Furthermore, can trigger macroautophagy/autophagy, a lysosome-dependent degradation pathway that plays dual role regulating survival or death fate cells under various stress conditions. Pathologically, impaired metabolism due to environmental genetic causes implicated variety human diseases, rare Wilson disease common cancers. Therapeutically, copper-based compounds are potential chemotherapeutic agents be used alone combination with other drugs approaches treat cancer. Here, we review progress made understanding metabolic processes their impact on regulation autophagy. This knowledge may help design future clinical tools improve cancer diagnosis treatment.

Language: Английский

Citations

299
Copper homeostasis and copper-induced cell death in the pathogenesis of cardiovascular disease and therapeutic strategies DOI Creative Commons
Xinyue Chen, Qi Cai, Ruikai Liang

et al.

Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(2)

Published: Feb. 11, 2023

Abstract Copper is a vital mineral, and an optimal amount of copper required to support normal physiologic processes in various systems, including the cardiovascular system. Over past few decades, copper-induced cell death, named cuproptosis, has become increasingly recognized as important process mediating pathogenesis progression disease (CVD), atherosclerosis, stroke, ischemia-reperfusion injury, heart failure. Therefore, in-depth understanding regulatory mechanisms cuproptosis CVD may be useful for improving management. Here, we review relationship between homeostasis cuproptosis-related pathways CVD, well therapeutic strategies addressing death CVD.

Language: Английский

Citations

148
Controlled Activation of TRPV1 Channels on Microglia to Boost Their Autophagy for Clearance of Alpha‐Synuclein and Enhance Therapy of Parkinson's Disease DOI
Jiaxin Yuan, Hanghang Liu, Hao Zhang

et al.

Advanced Materials, Journal Year: 2022, Volume and Issue: 34(11)

Published: Jan. 13, 2022

Parkinson's disease (PD) is characterized with accumulation of Lewy bodies a major component fibrillar alpha-synuclein (α-syn). Herein, boosting PD therapeutic efficacy by enhancing the autophagy microglia to phagocytose and degrade α-syn via controlled opening their surface TRPV1 channels rationally designed photothermal nanoagent reported. The Cu2-x Se-anti-TRPV1 nanoparticles (CS-AT NPs) are fabricated target open under second near infrared (NIR-II) laser irradiation cause influx Ca2+ activate ATG5 /CaMKK2/AMPK/mTOR signaling pathway, which promote phagocytosis degradation α-syn. CS-AT NPs efficiently delivered focused ultrasound into striatum mice high expression receptors. athletic ability treated NIR-II significantly improved due phagocytotic clearance enhanced autophagy. enzyme tyrosine hydroxylase, ionized calcium binding adapter protein 1, glial fibrillary acidic protein, pSer129-α-syn (p-α-syn) almost recovered normal levels healthy mice. This study provides insights activation microglial targeting ion improve treatment other neurodegenerative diseases.

Language: Английский

Citations

98
Copper in cancer: From pathogenesis to therapy DOI Open Access
Defeng Guan, Lihui Zhao, Xin Shi

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 163, P. 114791 - 114791

Published: April 25, 2023

One of the basic trace elements for structure and metabolism human tissue is copper. However, as a heavy metal, excessive intake or abnormal accumulation copper in body can cause inevitable damage to organism because result direct injury various cell components disruption redox balance, eventually leading death. Interestingly, growing research reports that diverse cancers have raised serum tumor levels. Tumor cells depend on more their than normal cells, decrease overload detrimental effect cells. New modalities identifying characterizing copper-dependent signals offer translational opportunities therapy, but mechanisms remain unclear. Therefore, this article summarizes what we currently know about correlation between cancer describes characteristics prospective application copper-derived therapeutics.

Language: Английский

Citations

64
Characterization, Anti-lung Cancer Activity, and Cytotoxicity of Bio-synthesized Copper Nanoparticles by Thymus fedtschenkoi Leaf Extract DOI

Ali Dehnoee,

Roozbeh Javad Kalbasi, Mohammad Mahdi Zangeneh

et al.

Journal of Cluster Science, Journal Year: 2023, Volume and Issue: unknown

Published: Nov. 28, 2023

Language: Английский

Citations

61
Copper in cancer: from limiting nutrient to therapeutic target DOI Creative Commons
Xiaolong Tang,

Zaihua Yan,

Yandong Miao

et al.

Frontiers in Oncology, Journal Year: 2023, Volume and Issue: 13

Published: June 23, 2023

As an essential nutrient, copper’s redox properties are both beneficial and toxic to cells. Therefore, leveraging the characteristics of copper-dependent diseases or using copper toxicity treat copper-sensitive may offer new strategies for specific disease treatments. In particular, concentration is typically higher in cancer cells, making a critical limiting nutrient cell growth proliferation. Hence, intervening metabolism cells become potential tumor treatment strategy, directly impacting metastasis. this review, we discuss body summarize research progress on role promoting inducing programmed death Additionally, elucidate copper-related drugs treatment, intending provide perspectives treatment.

Language: Английский

Citations

57
Recent Advances in Cancer Therapeutic Copper-Based Nanomaterials for Antitumor Therapy DOI Creative Commons
Reyida Aishajiang, Zhongshan Liu, Tiejun Wang

et al.

Molecules, Journal Year: 2023, Volume and Issue: 28(5), P. 2303 - 2303

Published: March 1, 2023

Copper serves as a vital microelement which is widely present in the biosystem, functioning multi-enzyme active site, including oxidative stress, lipid oxidation and energy metabolism, where reduction characteristics are both beneficial lethal to cells. Since tumor tissue has higher demand for copper more susceptible homeostasis, may modulate cancer cell survival through reactive oxygen species (ROS) excessive accumulation, proteasome inhibition anti-angiogenesis. Therefore, intracellular attracted great interest that multifunctional copper-based nanomaterials can be exploited diagnostics antitumor therapy. this review explains potential mechanisms of copper-associated death investigates effectiveness biomaterials field

Language: Английский

Citations

45
Copper homeostasis and cuproptosis in mitochondria DOI

Ziying Tian,

Su Jiang,

Jieyu Zhou

et al.

Life Sciences, Journal Year: 2023, Volume and Issue: 334, P. 122223 - 122223

Published: Oct. 29, 2023

Language: Английский

Citations

42
Heavy Metal Exposure: Molecular Pathways, Clinical Implications, and Protective Strategies DOI Creative Commons
Hajime Koyama, Teru Kamogashira, Tatsuya Yamasoba

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(1), P. 76 - 76

Published: Jan. 5, 2024

Heavy metals are often found in soil and can contaminate drinking water, posing a serious threat to human health. Molecular pathways curation therapies for mitigating heavy metal toxicity have been studied long time. Recent studies on oxidative stress aging shown that the molecular foundation of cellular damage caused by metals, namely, apoptosis, endoplasmic reticulum stress, mitochondrial share same as those involved senescence aging. In recent studies, many types exposures used both animal models. Chelation therapy is traditional treatment toxicity. However, recently, various antioxidants be effective treating metal-induced damage, shifting research focus investigating interplay between metals. this review, we introduce basis its relationship with aging, summarize clinical implications, discuss other agents protective effects against damage.

Language: Английский

Citations

32
Adenosine triphosphate-binding pocket inhibitor for mixed lineage kinase domain-like protein attenuated alcoholic liver disease via necroptosis-independent pathway DOI
Huiqing Yuan,

Hyun Sung Kim,

Gye Ryeol Park

et al.

World Journal of Gastroenterology, Journal Year: 2025, Volume and Issue: 31(6)

Published: Jan. 10, 2025

Mixed lineage kinase domain-like protein (MLKL) serves as a critical mediator in necroptosis, form of regulated cell death linked to various liver diseases. This study aims specifically investigate the role MLKL's adenosine triphosphate (ATP)-binding pocket facilitating necroptosis-independent pathways that may contribute disease progression. By focusing on this mechanism, we seek identify potential therapeutic targets can modulate MLKL activity, offering new strategies for prevention and treatment liver-related pathologies. To possibility using ATP-binding pocket-associated, pathway target Cell following necroptosis stimuli was evaluated proliferation assays, flow cytometry, electron microscopy cells. The human organoid system used evaluate whether ATP pocket-binding inhibitor could attenuate inflammation. Additionally, alcoholic non-alcoholic fatty diseases animal models were determine inhibitors injury. While an did not prevent necroptosis-induced RAW 264.7 cells, it reduce necroptosis-led expression CXCL2, ICAM, VCAM. Notably, diminishes VCAM by inhibiting IκB nuclear factor kappa-B without inducing two-dimensional culture well human-derived system. Although ineffective models, attenuated hepatic inflammation model. exerted anti-inflammatory effects through model disease.

Language: Английский

Citations

2