Disruption of the superoxide anions-mitophagy regulation axis mediates copper oxide nanoparticles-induced vascular endothelial cell death

Zhang, Jun; Wang, Bin; Wang, Hong; He, Hui; Wu, Qiong; Qin, Xia; Yang, Xi; Chen, Linmu; Xu, Guohai; Yuan, Zhiyi; Yi, Qiying; Zou, Zhen; Yu, Chao

doi:10.1016/j.freeradbiomed.2018.09.032

Cited by 42 publications

(32 citation statements)

References 55 publications

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“…Autophagy occurs and develops through a continuous dynamic process referred to as autophagic flux, which can be divided into five stages: initial, extension, autophagosome formation, autophagosome and lysosome fusion, and degradation in lysosomes [14]. Normal autophagy can remove abnormally synthesized proteins in cells and digest damaged and redundant organelles, which is beneficial for intracellular homeostasis.…”

Section: The Involvement Of Autophagy Dysfunction In Organelle Impairmentioning

confidence: 99%

“…Conversely, GO-Ag NPs were detected to cause mitochondrial damage such as a decrease in mitochondrial membrane potential (MMP) in the first step, and further accelerate the progression of autophagy dysfunction [137]. Based on these results, the authors referred to mitophagy as a direct mechanism connecting mitochondrial disorder to (macro) autophagy, which can maintain mitochondrial homeostasis through clearance of damaged mitochondria and excessive superoxide anions [14]. Similar findings were also demonstrated in SiNP-treated human umbilical vein endothelial cells (HUVECs), which were manifested by decreased mitochondrial activity and membrane integrity that subsequently led to size-dependent mitophagy [138].…”

Section: Mitochondrial Disruptionmentioning

confidence: 99%

“…For these considerations, a large number of studies have investigated the biological hazard of NMs through varying exposure pathways [10][11][12][13]. In view that NMs are more chemically active than their bulk counterparts, NMs distributed in different organs can cause distinct toxic effects through interacting with cells, proteins, or DNA after entering the body [14][15][16][17]. At present, the most widely investigated mechanisms of NM-driven toxicity include oxidative stress, inflammatory response and cell apoptosis, but other underlying mechanisms remain obscure and require our particular attention [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

“…Nanomaterials, especially those with a smaller particle size (<20 nm), are excreted mainly through the kidney in vivo [ 14 ]; thus, there is a great possibility that they will accumulate in the kidney and further cause adverse effects such as renal fibrosis or inflammation [ 109 , 110 ]. Jiang et al [ 111 ] found that intravenously injected cadmium telluride quantum dots were mostly distributed in the kidney of mice and triggered unfolded protein response (UPR)-mediated endoplasmic reticulum autophagy, leading to renal dysfunction.…”

Section: Introductionmentioning

confidence: 99%

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Nanomaterial-mediated autophagy: coexisting hazard and health benefits in biomedicine

Feng

Zhang

et al. 2020

Part Fibre Toxicol

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Background Widespread biomedical applications of nanomaterials (NMs) bring about increased human exposure risk due to their unique physicochemical properties. Autophagy, which is of great importance for regulating the physiological or pathological activities of the body, has been reported to play a key role in NM-driven biological effects both in vivo and in vitro. The coexisting hazard and health benefits of NM-mediated autophagy in biomedicine are nonnegligible and require our particular concerns. Main body We collected research on the toxic effects related to NM-mediated autophagy both in vivo and in vitro. Generally, NMs can be delivered into animal models through different administration routes, or internalized by cells through different uptake pathways, exerting varying degrees of damage in tissues, organs, cells, and organelles, eventually being deposited in or excreted from the body. In addition, other biological effects of NMs, such as oxidative stress, inflammation, necroptosis, pyroptosis, and ferroptosis, have been associated with autophagy and cooperate to regulate body activities. We therefore highlight that NM-mediated autophagy serves as a double-edged sword, which could be utilized in the treatment of certain diseases related to autophagy dysfunction, such as cancer, neurodegenerative disease, and cardiovascular disease. Challenges and suggestions for further investigations of NM-mediated autophagy are proposed with the purpose to improve their biosafety evaluation and facilitate their wide application. Databases such as PubMed and Web of Science were utilized to search for relevant literature, which included all published, Epub ahead of print, in-process, and non-indexed citations. Conclusion In this review, we focus on the dual effect of NM-mediated autophagy in the biomedical field. It has become a trend to use the benefits of NM-mediated autophagy to treat clinical diseases such as cancer and neurodegenerative diseases. Understanding the regulatory mechanism of NM-mediated autophagy in biomedicine is also helpful for reducing the toxic effects of NMs as much as possible.

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Section: The Involvement Of Autophagy Dysfunction In Organelle Impairmentioning

confidence: 99%

Section: Mitochondrial Disruptionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nanomaterial-mediated autophagy: coexisting hazard and health benefits in biomedicine

Feng

Zhang

et al. 2020

Part Fibre Toxicol

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“…ODS removes superoxide radicals and prevents the formation of other more dangerous to the body free radicals: hydroxyl radical and singlet oxygen. In addition, SOD prevents the accumulation of neutrophils in the inflammation zone, which secrete significant amounts of lysosomal enzymes that destroy nearby tissues [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Correlation of the distribution of antioxidant enzyme concentrations in blood serum and heart tissue in rats

et al. 2020

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Cardiovascular diseases have been the leading cause of death worldwide for many years. In recent years, new cardiovascular disease markers have been sought that can improve the diagnosis and treatment of this broad and prognostically unfavorable group of diseases. The efforts of many researchers are aimed at detecting changes in the level of enzymes in the lipid peroxidation system, which are antioxidants, as possible mechanisms underlying the development of cardiovascular disease. The imbalance between the intensification of free-radical oxidation caused by active oxygen forms and the activity of the body’s protective antioxidant system leads to serious disturbances: disorganization of cellular structures, changes in their functional activity. The article presents the study of the interrelation of the concentration distribution of enzymes of the lipid peroxidation system – antioxidants in blood serum and heart tissues of white non-pedigree rats. The correlation coefficients of Spearman, the gamma of correlation and Kendel Tau revealed a reliable presence of weak correlation between the concentration of glutathione peroxidase in blood serum and heart tissues (Spearman R = 0.18 at p ≤ 0.029408, Gamma = 0.14 at p ≤ 0.018701; Kendall Tau = 0.13 at p ≤ 0.018701).

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Mitophagy and its regulatory mechanisms in the biological effects of nanomaterials

Zhang,

Yang,

Guo

et al. 2024

J of Applied Toxicology

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Mitophagy is a selective cellular process critical for the removal of damaged mitochondria. It is essential in regulating mitochondrial number, ensuring mitochondrial functionality, and maintaining cellular equilibrium, ultimately influencing cell destiny. Numerous pathologies, such as neurodegenerative diseases, cardiovascular disorders, cancers, and various other conditions, are associated with mitochondrial dysfunctions. Thus, a detailed exploration of the regulatory mechanisms of mitophagy is pivotal for enhancing our understanding and for the discovery of novel preventive and therapeutic options for these diseases. Nanomaterials have become integral in biomedicine and various other sectors, offering advanced solutions for medical uses including biological imaging, drug delivery, and disease diagnostics and therapy. Mitophagy is vital in managing the cellular effects elicited by nanomaterials. This review provides a comprehensive analysis of the molecular mechanisms underpinning mitophagy, underscoring its significant influence on the biological responses of cells to nanomaterials. Nanoparticles can initiate mitophagy via various pathways, among which the PINK1‐Parkin pathway is critical for cellular defense against nanomaterial‐induced damage by promoting mitophagy. The role of mitophagy in biological effects was induced by nanomaterials, which are associated with alterations in Ca2+ levels, the production of reactive oxygen species, endoplasmic reticulum stress, and lysosomal damage.

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Disruption of the superoxide anions-mitophagy regulation axis mediates copper oxide nanoparticles-induced vascular endothelial cell death

Cited by 42 publications

References 55 publications

Nanomaterial-mediated autophagy: coexisting hazard and health benefits in biomedicine

Nanomaterial-mediated autophagy: coexisting hazard and health benefits in biomedicine

Correlation of the distribution of antioxidant enzyme concentrations in blood serum and heart tissue in rats

Mitophagy and its regulatory mechanisms in the biological effects of nanomaterials

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