Inhibition of ferroptosis alleviates atherosclerosis through attenuating lipid peroxidation and endothelial dysfunction in mouse aortic endothelial cell

Bai, Tao; Li, Mingxing; Liu, Yuanfeng; Qiao, Zhentao; Wang, Zhiwei

doi:10.1016/j.freeradbiomed.2020.07.026

Cited by 292 publications

(273 citation statements)

References 53 publications

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“…GPX4 can inhibit ferroptosis by scavenging lipid peroxides and improve the function of the heart [58][59][60]. GPX4 overexpression inhibits atherosclerosis in ApoE -/mice [61,62]. Hyperglycemia can increase the production of ROS, such as O 2 − and peroxide, through the mitochondrial electron transport chain, and then form a positive feedback effect [63,64].…”

Section: Atherosclerosismentioning

confidence: 99%

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Wang

Dong

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Reduction oxidation (REDOX) reaction is crucial in life activities, and its dynamic balance is regulated by ROS. Reactive oxygen species (ROS) is associated with a variety of metabolic diseases involving in multiple cellular signalling in pathologic and physiological signal transduction. ROS are the by-products of numerous enzymatic reactions in various cell compartments, including the cytoplasm, cell membrane, endoplasmic reticulum (ER), mitochondria, and peroxisome. ROS signalling is not only involved in normal physiological processes but also causes metabolic dysfunction and maladaptive responses to inflammatory signals, which depends on the cell type or tissue environment. Excess oxidants are able to alter the normal structure and function of DNA, lipids, and proteins, leading to mutations or oxidative damage. Therefore, excessive oxidative stress is usually regarded as the cause of various pathological conditions, such as cancer, neurodegeneration, cardiovascular diseases (CVDs), diabetes, and kidney diseases. Currently, it has been possible to detect diabetes and other cardiac diseases by detecting derivatives accompanied by oxidative stress in vivo as biomarkers, but there is no effective method to treat these diseases. In consequence, it is essential for us to seek new therapy targeting these diseases through understanding the role of ROS signalling in regulating metabolic activity, inflammatory activation, and cardiac diseases related to metabolic dysfunction. In this review, we summarize the current literature on REDOX and its role in the regulation of cardiac metabolism and inflammation, focusing on ROS, local REDOX signalling pathways, and other mechanisms.

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Section: Atherosclerosismentioning

confidence: 99%

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Wang

Dong

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Ferroptosis is a new form of non-apoptotic cell death marked by the oxidative modification of phospholipid membranes via an iron-dependent mechanism [ 14 ]. Although the physiological function of ferroptosis is poorly understood, its implication in several human diseases such as tumorigenesis [ 15 , 16 ], CVDs (e.g., atherosclerosis [ 17 ], ischemia-reperfusion injury (IRI) [ 18 ], cardiomyopathy [ 19 , 20 ], and heart failure [ 21 ]) has been widely reported.…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis: a cell death connecting oxidative stress, inflammation and cardiovascular diseases

et al. 2021

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Ferroptosis, a recently identified and iron-dependent cell death, differs from other cell death such as apoptosis, necroptosis, pyroptosis, and autophagy-dependent cell death. This form of cell death does not exhibit typical morphological and biochemical characteristics, including cell shrinkage, mitochondrial fragmentation, nuclear condensation. The dysfunction of lipid peroxide clearance, the presence of redox-active iron as well as oxidation of polyunsaturated fatty acid (PUFA)-containing phospholipids are three essential features of ferroptosis. Iron metabolism and lipid peroxidation signaling are increasingly recognized as central mediators of ferroptosis. Ferroptosis plays an important role in the regulation of oxidative stress and inflammatory responses. Accumulating evidence suggests that ferroptosis is implicated in a variety of cardiovascular diseases such as atherosclerosis, stroke, ischemia-reperfusion injury, and heart failure, indicating that targeting ferroptosis will present a novel therapeutic approach against cardiovascular diseases. Here, we provide an overview of the features, process, function, and mechanisms of ferroptosis, and its increasingly connected relevance to oxidative stress, inflammation, and cardiovascular diseases.

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“…Studies showed that after 24 weeks of iron consumption, both ND-fed and HCD-fed zebrafish displayed significant increases in serum cholesterol and triglyceride levels, which for the first time demonstrated the influence of iron consumption on lipid homeostasis in a zebrafish model (Kim et al, 2017). It was reported that inhibition of ferroptosis alleviated AS in ApoE −/− mice, through attenuating lipid peroxidation and endothelial dysfunction in aortic endothelial cell (Bai et al, 2020). However, there is no report on ferroptosis in zebrafish AS models yet.…”

Section: Trace Elementsmentioning

confidence: 90%

Recent Application of Zebrafish Models in Atherosclerosis Research

Tang

Geng

et al. 2021

Front. Cell Dev. Biol.

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Atherosclerotic cardiovascular disease is one of the leading causes of death worldwide. Establishing animal models of atherosclerosis is of great benefit for studying its complicated pathogenesis and screening and evaluating related drugs. Although researchers have generated a variety of models for atherosclerosis study in rabbits, mice and rats, the limitations of these models make it difficult to monitor the development of atherosclerosis, and these models are unsuitable for large scale screening of potential therapeutic targets. On the contrast, zebrafish can fulfill these purposes thanks to their fecundity, rapid development ex utero, embryonic transparency, and conserved lipid metabolism process. Thus, zebrafish have become a popular alternative animal model for atherosclerosis research. In this mini review, we summarize different zebrafish models used to study atherosclerosis, focusing on the latest applications of these models to the dynamic monitoring of atherosclerosis progression, mechanistic study of therapeutic intervention and drug screening, and assessment of the impacts of other risk factors.

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Inhibition of ferroptosis alleviates atherosclerosis through attenuating lipid peroxidation and endothelial dysfunction in mouse aortic endothelial cell

Cited by 292 publications

References 53 publications

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Ferroptosis: a cell death connecting oxidative stress, inflammation and cardiovascular diseases

Recent Application of Zebrafish Models in Atherosclerosis Research

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