Cu(OH)2 nanopesticide induced liver dysfunction in mice by targeting lipoylated tricarboxylic acid cycle proteins via ferredoxin 1

Journal of Hazardous Materials, Journal Year: 2025, Volume and Issue: 494, P. 138403 - 138403

Published: April 25, 2025

Language: Английский

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Ferroptosis: action and mechanism of chemical/drug-induced liver injury

Drug and Chemical Toxicology, Journal Year: 2023, Volume and Issue: unknown, P. 1 - 12

Published: Dec. 26, 2023

Drug-induced liver injury (DILI) is characterized by hepatocyte injury, cholestasis and mixed injury. The transplantation required for serious clinical outcomes such as acute failure. Current studies have found that many mechanisms were involved in DILI, mitochondrial oxidative stress, apoptosis, necroptosis, autophagy, ferroptosis, etc. Ferroptosis occurs when hepatocytes die from iron-dependent lipid peroxidation plays a key role DILI. After entry into the liver, where some drugs or chemicals are metabolized, they convert hepatotoxic substances, consume reduced glutathione (GSH), decrease reductive capacity of GSH-dependent GPX4, leading to redox imbalance increase reactive oxygen species (ROS) level, undermining hepatocytes; facilitated autophagy ferritin, orchestrating increased ion level ferroptosis. purpose this review summarize ferroptosis chemical- drug-induced (chemical/DILI) how natural products inhibit prevent chemical/DILI.

Language: Английский

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Mitochondrial miR-12294-5p-Regulated Copper Exposure-Caused Mitochondrial-Dependent Ferroptosis by Targeted Inhibition of CISD1 in Chicken Hepatocytes

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(28), P. 15948 - 15958

Published: July 5, 2024

Copper (Cu) is a common trace element additive in animal and human foods, excessive intake of Cu has been shown to cause hepatotoxicity, but the underlying mechanism remains unclear. Our previous research found that exposure dramatically upregulated mitochondrial miR-12294-5p expression confirmed its targeted inhibition CISD1 chicken hepatocytes. Thus, we aimed explore potential role mitomiR-12294-5p/CISD1 axis exposure-resulted hepatotoxicity. Here, observed resulted accumulation pathological injury livers. Moreover, caused mitochondrial-dependent ferroptosis hepatocytes, which were prominent on increased Fe2+ lipid peroxidation, inhibited levels CISD1, GPX4, DHODH, IDH2, also enhanced level PTGS2. Notably, identified mitomiR-2954 effectively mitigated Cu-exposure-resulted peroxidation prevented development ferroptosis. However, increasing mitomiR-12294-5p considerably aggravated influence these indicators. Meanwhile, overexpression alleviated Cu-caused ferroptosis, while silent eliminated therapeutic inhibitor. Overall, our findings indicated played critical function hepatotoxicity chickens by regulating

Language: Английский

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Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(21), P. 11462 - 11462

Published: Oct. 25, 2024

Cardiovascular disease (CVD) is a leading cause of death globally, with atherosclerosis (AS) playing central role in its pathogenesis as chronic inflammatory condition. Copper, an essential trace element the human body, participates various biological processes and plays significant cardiovascular system. Maintaining normal copper homeostasis crucial for health, dysregulation balance closely associated development CVD. When disrupted, it can induce cell death, which has been proposed to be novel form "cuproptosis", distinct from traditional programmed death. This new linked occurrence progression AS. article elaborately describes physiological mechanisms explores interactions signaling pathways related Additionally, we focus on process mechanism induced by imbalances summarize relationship between homeostasis-related genes We also emphasize potential therapeutic approaches, such regulators nanotechnology interventions, adjust levels providing ideas strategies prevention treatment

Language: Английский

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Recent Advances in Nanomaterial‐Mediated Cell Death for Cancer Therapy

Advanced Healthcare Materials, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 5, 2024

Abstract Nanomedicine has shown great anticancer potential by disrupting redox homeostasis and increasing the levels of oxidative stress, but therapeutic effect is limited factors including intrinsic self‐protection mechanism tumors. Cancer cell death can be induced exploration different mechanisms, such as apoptosis, pyroptosis, necroptosis, cuproptosis, ferroptosis. The merging nanotechnology with biomedicine provided tremendous opportunities to construct death‐based nanomedicine for innovative cancer therapy. Nanocarriers are not only used targeted delivery inducers, also components induce achieve efficient tumor treatment. This review focuses on seven modalities mediated nanomaterials, ferroptosis, cuprotosis, immunogenic death, autophagy. mechanisms these described in detail, well preparation nanomaterials that them they exert their effects. Finally, this work describes future development based current knowledge related nanomaterials.

Language: Английский

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