Ferroptosis Signaling and Regulators in Atherosclerosis

Zhao, Yajie; Ye, Ting; Yang, Liming; Shen, Yanna; Li, Hong

doi:10.3389/fcell.2021.809457

Cited by 64 publications

(40 citation statements)

References 144 publications

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“…Hence, oxidative stress has become a critical linking between ferroptosis and neurological disorders. Up to now, the inhibitors and activators of ferroptosis [9][10][11][12][13][14], as well as other involved signaling pathways [15][16][17], have been widely studied. Furthermore, the mediators of oxidative stress might become a potential therapeutic target for the treatment of neurological disorders by regulating the process of ferroptosis.…”

Section: Introductionmentioning

confidence: 99%

Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders

Jia

Cheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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With the acceleration of population aging, nervous system diseases including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), anxiety, depression, stroke, and traumatic brain injury (TBI) have become a huge burden on families and society. The mechanism of neurological disorders is complex, which also lacks effective treatment, so relevant research is required to solve these problems urgently. Given that oxidative stress-induced lipid peroxidation eventually leads to ferroptosis, both oxidative stress and ferroptosis are important mechanisms causing neurological disorders, targeting mediators of oxidative stress and ferroptosis have become a hot research direction at present. Our review provides a current view of the mechanisms underlying ferroptosis and oxidative stress participate in neurological disorders, the potential application of molecular mediators targeting ferroptosis and oxidative stress in neurological disorders. The target of molecular mediators or agents of oxidative stress and ferroptosis associated with neurological disorders, such as reactive oxygen species (ROS), nuclear factor erythroid 2–related factor-antioxidant response element (Nrf2-ARE), n-acetylcysteine (NAC), Fe2+, NADPH, and its oxidases NOX, has been described in this article. Given that oxidative stress-induced ferroptosis plays a pivotal role in neurological disorders, further research on the mechanisms of ferroptosis caused by oxidative stress will help provide new targets for the treatment of neurological disorders.

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Section: Introductionmentioning

confidence: 99%

Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders

Jia

Cheng

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Ferroptosis, a newly discovered way of iron-dependent oxidative cell death, was realized though the regulation of lipid peroxidation ( Wang et al, 2021a ; Chen et al, 2021 ). An increasing body of evidence has suggested the functional roles of ferroptosis in CRC tumorigenesis and treatment ( Tang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis-Related Gene MT1G as a Novel Biomarker Correlated With Prognosis and Immune Infiltration in Colorectal Cancer

Peng

Kang

et al. 2022

Front. Cell Dev. Biol.

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Ferroptosis, a newly discovered way of cell death, has been proved to be involved in the oncogenesis and development of cancers, including colorectal cancer (CRC). Here, by identifying the differentially expressed genes (DEGs) from three CRC transcriptome microarray datasets (GSE20842, GSE23878, and GSE25070), we found that the expression of MT1G was significantly decreased in CRC tissues, and the patients with a high level of MT1G displayed a poor prognosis. Quantitative PCR (qPCR) further confirmed the downregulated MT1G in two CRC cells, HCT8 and HCT116. The colony-forming assay indicated that the MT1G overexpression exhibited a remarkable inhibition of cell proliferation in HCT8 and HCT116 cells. In addition, we explored the co-expressed genes of MT1G to gain a better understanding of its potential signaling pathways. Aberrantly expressed MT1G also affected the immune response of CRC patients. Collectively, these findings might deepen our comprehension on the potential biological implications of MT1G in CRC.

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“…Following cerebral ischemia, the release of inflammatory cytokines and neurotoxic mediators can be induced through multiple signaling pathways, such as NF-κB and STAT3, leading to neuronal damage and death (113). NF-κB activation following ischemia, and the expression of TNF-α, IL-1 and IL-6, is upregulated in cells to promote the inflammatory response (11). The high expression of IL-6 promotes the continuous phosphorylation of signal transducers and STAT3, and the transcription factor NF-κB enters the nucleus from the cytoplasm, regulating the expression of inflammatory cytokines, causing endothelial cell dysfunction and macrophage polarization, and promoting inflammation (114).…”

Section: Ferroptosis Accelerates the Progression Of As Leading To Isc...mentioning

confidence: 99%

“…Therefore, ferroptosis may be a key factor in the occurrence and development of AS. Ferroptosis is associated with various stages of AS development through numerous physiological mechanisms, such as iron ion metabolism, lipid metabolism and amino acid metabolism (11). Atherosclerotic stenosis is the root cause of vascular-related diseases, such as coronary heart disease, stroke and peripheral vascular disease.…”

Section: Introductionmentioning

confidence: 99%

Potential intervention target of atherosclerosis: Ferroptosis (Review)

Zuo

et al. 2022

Mol Med Rep

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Atherosclerosis (AS) is a chronic inflammatory disease of the blood vessels, which is mainly characterized by the form of atherosclerotic plaques and vascular endothelial injury. Its formation involves abnormal lipid metabolism, oxidative stress and inflammation, as well as other processes. AS is the direct cause of various acute cardiovascular and cerebrovascular diseases, such as acute myocardial infarction and acute ischemic stroke. Early intervention in the atherosclerotic inflammatory process and lesion progression is beneficial, and has been associated with the primary prevention of a range of related diseases. Ferroptosis is a non-apoptotic form of cell death different from cell necrosis and autophagy, which has been shown to participate in atherogenesis and atherosclerotic progression through numerous signaling pathways. The main characteristic of ferroptosis is the formation of high levels of cellular iron catalytic free radicals, unsaturated fatty acid accumulation and iron-induced lipid reactive oxygen species accumulation, which can cause oxidative stress, and subsequent DNA, protein and lipid damage. There are numerous hypotheses about the pathogenesis of AS. At present, it has been suggested that ferroptosis can accelerate the progression of AS and that inflammation is associated with the whole process of AS. The mechanisms and signaling pathways related to the involvement of neuroinflammation and ferroptosis in the progression of AS, and therapeutic targets associated with ferroptosis have not yet been elucidated. The present review article evaluated the involvement of ferroptosis in the progression of AS from the perspectives of ferroptotic cell death, the pathogenesis of AS and nervous system inflammation, with the aim of exploring new therapeutic targets for AS. Contents1. Introduction 2. Iron and ferroptosis 3. Ferroptosis is involved in the formation and progression of AS 4. Ferroptosis accelerates the progression of AS, leading to ischemic stroke 5. Conclusion and future perspectives

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Ferroptosis Signaling and Regulators in Atherosclerosis

Cited by 64 publications

References 144 publications

Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders

Targeting Molecular Mediators of Ferroptosis and Oxidative Stress for Neurological Disorders

Ferroptosis-Related Gene MT1G as a Novel Biomarker Correlated With Prognosis and Immune Infiltration in Colorectal Cancer

Potential intervention target of atherosclerosis: Ferroptosis (Review)

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