Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Zhou, Yue; Liao, Jun; Mei, Zhigang; Liu, Xun; Ge, Jinwen

doi:10.1155/2021/9991001

Cited by 83 publications

(65 citation statements)

References 204 publications

(312 reference statements)

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“…That means ferroptosis still occurs frequently in recent necroptosis studies, indicating that the cross-talk between necroptosis and ferroptosis might be a new rising research area. Multiple structural, functional, and mechanistic evidence proved their cross-talk ( 60 ). One of the mechanisms of ferroptosis is that iron overload leads to a mitochondrial permeability transition pore (MPTP) opening, which exacerbates RIPK1 phosphorylation and contributes to necroptosis ( 61 , 62 ).…”

Section: Discussionmentioning

confidence: 99%

Knowledge Mapping of Necroptosis From 2012 to 2021: A Bibliometric Analysis

et al. 2022

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BackgroundNecroptosis, a recently discovered programmed cell death, has been pathologically linked to various diseases and is thus a promising target for treating diseases. However, a comprehensive and objective report on the current status of entire necroptosis research is lacking. Therefore, this study aims to conduct a bibliometric analysis to quantify and identify the status quo and trending issues of necroptosis research in the last decade.MethodsArticles were acquired from the Web of Science Core Collection database. We used two bibliometric tools (CiteSpace and VOSviewer) to quantify and identify the individual impact and cooperation information by analyzing annual publications, journals, co-cited journals, countries/regions, institutions, authors, and co-cited authors. Afterwards, we identified the trending research areas of necroptosis by analyzing the co-occurrence and burst of keywords and co-cited references.ResultsFrom 2012 to 2021, a total of 3,111 research articles on necroptosis were published in 786 academic journals by 19,687 authors in 885 institutions from 82 countries/regions. The majority of publications were from China and the United States, of which the United States maintained the dominant position in necroptosis research; meanwhile, the Chinese Academy of Sciences and Ghent University were the most active institutions. Peter Vandenabeele published the most papers, while Alexei Degterev had the most co-citations. Cell Death & Disease published the most papers on necroptosis, while Cell was the top 1 co-cited journal, and the major area of these publications was molecular, biology, and immunology. High-frequency keywords mainly included those that are molecularly related (MLKL, TNF-alpha, NF-κB, RIPK3, RIPK1), pathological process related (cell-death, apoptosis, necroptosis, necrosis, inflammation), and disease related (cancer, ischemia/reperfusion injury, infection, carcinoma, Alzheimer’s disease).ConclusionNecroptosis research had a stable stepwise growth in the past decade. Current necroptosis studies focused on its cross-talk with other types of cell death, potential applications in disease treatment, and further mechanisms. Among them, the synergy with ferroptosis, further RIPK1/RIPK3/MLKL studies, its association with inflammation and oxidative stress and translational applications, and the therapeutic potential to treat cancer and neurodegenerative diseases are the trending research area. These might provide ideas for further research in the necroptosis field.

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Section: Discussionmentioning

confidence: 99%

Knowledge Mapping of Necroptosis From 2012 to 2021: A Bibliometric Analysis

et al. 2022

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“…Cell death, especially apoptosis, has been demonstrated as a hallmark after SAH during the past few decades [ 6 , 7 ]. Ferroptosis, characterized by iron-dependent lipid peroxidation, is a new form of programmed cell death, which differs from apoptosis or necroptosis [ 8 , 9 ]. The morphological features of a ferroptotic cell are shrunken mitochondria with increased mitochondrial membrane density, a reduction of mitochondria crista, and outer membrane rupture [ 8 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

Cepharanthine Attenuates Early Brain Injury after Subarachnoid Hemorrhage in Mice via Inhibiting 15-Lipoxygenase-1-Mediated Microglia and Endothelial Cell Ferroptosis

Gao

Zhou

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Ferroptosis is a newly identified form of programmed cell death caused by iron-dependent lipid peroxidation. Our study was designed to determine the expression patterns and role of 15-lipoxygenase-1 (ALOX15) in subarachnoid hemorrhage (SAH) and to investigate whether cepharanthine (CEP) can inhibit ferroptosis by inhibiting ALOX15 in specific cell types. Methods. A mouse model of SAH was developed by the endovascular perforation method. bEend.3 endothelial cells and BV2 microglial cells as well as RSL3 and hemin were used to simulate SAH in vitro. Mice and cell lines were treated with CEP and a group of specific oxygenase inhibitors to explore the protection effect from ferroptosis. Lipid peroxidation staining with BODIPY 581/591 C11 and transmission electron microscopy were used to identify ferroptosis in vitro and in vivo. Results. In the present study, the accumulation of lipid peroxide, a defect in the glutathione peroxidase 4 (GPx4)/glutathione (GSH) antioxidant system, highly expressed ALOX15 in microglia and endothelium, and ferroptotic changes in microglial mitochondria confirmed the occurrence of ferroptosis after SAH in vivo. Further, CEP was shown to inhibit ferroptosis and improve neurological function by downregulating the expression of ALOX15. During in vitro experiments, we investigated the important role ALOX15 in RSL3-induced endothelial ferroptosis. In addition, we found that M2-type microglia are more sensitive to RSL3-induced ferroptosis than M1-type microglia and that hemin probably induced ferroptosis in M2-type microglia by increasing ALOX15 levels and decreasing GPx4 levels. The effect of CEP treatment was also demonstrated in vitro. Conclusions. In summary, to the best of our knowledge, this is the first study demonstrating that ferroptosis occurred in the microglia and endothelium after SAH, and this process was facilitated by increased ALOX15 levels. More importantly, treatment with CEP could inhibit ferroptosis through downregulating the expression of ALOX15.

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“…Heat shock protein 90 (HSP90) is defined as a common regulatory nodal between ferroptosis and necroptosis ( Wu et al, 2019 ). Friedmann Angeli et al demonstrated that necrostatin-1 (RIP1 inhibitor) inhibits ferroptosis through a necroptosis/RIP1-independent manner, but ferroptosis inhibitors cannot inhibit necroptosis ( Friedmann Angeli et al, 2014 ) and the specific link between ferroptosis and necroptosis remains to be clarified after stroke ( Zille et al, 2017 ; Zhou et al, 2021 ). Carthamin yellow attenuates cerebral I/R injury via suppressing NF-κB/NLRP3-mediated pyroptosis and ACSL4-mediated ferroptosis in rats ( Guo et al, 2021b ).…”

Section: Discussionmentioning

confidence: 99%

Bibliometric Analysis of Ferroptosis in Stroke From 2013 to 2021

Chen

Long

et al. 2022

Front. Pharmacol.

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Background: Stroke is a major cause of long-term disability and death, but the clinical therapeutic strategy for stroke is limited and more research must be conducted to explore the possible avenues for stroke treatment and recovery. Since ferroptosis is defined, its role in the body has become the focus of attention and discussion, including in stroke.Methods: In this work, we aim to systematically discuss the “ferroptosis in stroke” research by bibliometric analysis. Documents were retrieved from the Web of Science Core Collection database on October 30, 2021. Statistical analysis and visualization analysis were conducted by the VOSviewer 1.6.15.Results: Ninety-nine documents were identified for bibliometric analysis. Research on “ferroptosis in stroke” has been rapidly developing and has remained the focus of many scholars and organizations in the last few years, but the Chinese groups in this field still lacked collaboration with others. Documents and citation analysis suggested that Rajiv R. Ratan and Brent R. Stockwell are active researchers, and the research by Qingzhang Tuo, Ishraq Alim, and Qian Li are more important drivers in the development of the field. Keywords associated with lipid peroxidation, ferroptosis, iron, oxidative stress, and cell death had high frequency, but apoptosis, necroptosis, pyroptosis, and autophagy had scant research, and there may be more research ideas in the future by scholars.Conclusion: Further exploration of the mechanisms of crosstalk between ferroptosis and other programmed cell death may improve clinical applications and therapeutic effects against stroke. Scholars will also continue to pay attention to and be interested in the hot topic “ferroptosis in stroke”, to produce more exciting results and provide new insights into the bottleneck of stroke treatment.

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Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Cited by 83 publications

References 204 publications

Knowledge Mapping of Necroptosis From 2012 to 2021: A Bibliometric Analysis

Knowledge Mapping of Necroptosis From 2012 to 2021: A Bibliometric Analysis

Cepharanthine Attenuates Early Brain Injury after Subarachnoid Hemorrhage in Mice via Inhibiting 15-Lipoxygenase-1-Mediated Microglia and Endothelial Cell Ferroptosis

Bibliometric Analysis of Ferroptosis in Stroke From 2013 to 2021

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