Mitochondrial ferritin attenuates cerebral ischaemia/reperfusion injury by inhibiting ferroptosis

Wang, Peina; Cui, Yunxia; Ren, Qianqian; Yan, Bingqi; Zhao, Ya-Shuo; Yu, Peng; Gao, Guofen; Shi, Honglian; Chang, Shiyang; Chang, Yan‐Zhong

doi:10.1038/s41419-021-03725-5

Cited by 117 publications

(85 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Wang et al [ 87 ] reported that FtMt levels upregulate in the ischemic brains of mice. Moreover, mice lacking FtMt experience more severe brain damage and neurological deficits, accompanied by the typical molecular features of ferroptosis (increased lipid peroxidation) after cerebral ischemia-reperfusion (I/R), suggesting that FtMt plays a critical role in protecting against cerebral I/R [ 87 ].…”

Section: Mitochondrial Antioxidant Systemmentioning

confidence: 99%

Mitochondrial Management of Reactive Oxygen Species

Napolitano

Fasciolo²,

Venditti³

2021

Antioxidants

100

View full text Add to dashboard Cite

Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

show abstract

Section: Mitochondrial Antioxidant Systemmentioning

confidence: 99%

Mitochondrial Management of Reactive Oxygen Species

Napolitano

Fasciolo²,

Venditti³

2021

Antioxidants

100

View full text Add to dashboard Cite

show abstract

“…In addition, Rosaria et al ( Ingrassia et al, 2012 ) observed increased expression of NF-κB-regulated 1B isoform of the divalent metal transporter-1 (1B/DMT1) in animal and cellular models of ischemic stroke, which was associated with increased iron uptake into neuronal cells. Recently, Wang et al reported that mitochondrial ferritin attenuates neuronal ferroptosis by decreasing the intracellular labile iron pool during cerebral IR injury ( Wang et al, 2021 ).…”

Section: Mechanisms Of Ferroptosis In the Pathogenesis Of Ischemic Strokementioning

confidence: 99%

Emerging Role of Ferroptosis in the Pathogenesis of Ischemic Stroke: A New Therapeutic Target?

Wang

et al. 2021

ASN Neuro

View full text Add to dashboard Cite

Ischemic stroke is one of the main causes of high morbidity, mortality, and disability worldwide; however, the treatment methods are limited and do not always achieve satisfactory results. The pathogenesis of ischemic stroke is complex, defined by multiple mechanisms; among them, programmed death of neuronal cells plays a significant role. Ferroptosis is a novel type of regulated cell death characterized by iron redistribution or accumulation and increased lipid peroxidation in the membrane. Ferroptosis is implicated in many pathological conditions, such as cancer, neurodegenerative diseases, and ischemia-reperfusion injury. In this review, we summarize current research findings on ferroptosis, including possible molecular mechanisms and therapeutic applications of ferroptosis regulators, with a focus on the involvement of ferroptosis in the pathogenesis and treatment of ischemic stroke. Understanding the role of ferroptosis in ischemic stroke will throw some light on the development of methods for diagnosis, treatment, and prevention of this devastating disease.

show abstract

“…With the deepening of research, the regulatory network of ferroptosis in stroke is gradually revealed ( Bai et al, 2020 ; DeGregorio-Rocasolano, et al, 2019 ; Zille et al, 2017 ). Ferritin reduces robust ROS production and GSH consumption; its decrease is necessary for cerebral ischemia-induced hippocampal neuronal ferroptosis through p53 and SLC7A11 in middle cerebral artery occlusion (MCAO) rats ( Chen W. et al, 2021 ), and mice lacking mitochondrial ferritin show graver brain injury and neurological deficits, accompanied by typical ferroptotic event after cerebral ischemia/reperfusion (I/R) ( Wang et al, 2021 ). ACSL4 enhances ischemic stroke by increasing ferroptosis-induced brain damage and neuroinflammation while inhibiting ACSL4, which promotes the recovery of neurological function following stroke ( Li et al, 2019 ; Chen J. et al, 2021 ; Cui et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Bibliometric Analysis of Ferroptosis in Stroke From 2013 to 2021

Chen

Long

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

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.

show abstract

Mitochondrial ferritin attenuates cerebral ischaemia/reperfusion injury by inhibiting ferroptosis

Cited by 117 publications

References 60 publications

Mitochondrial Management of Reactive Oxygen Species

Mitochondrial Management of Reactive Oxygen Species

Emerging Role of Ferroptosis in the Pathogenesis of Ischemic Stroke: A New Therapeutic Target?

Bibliometric Analysis of Ferroptosis in Stroke From 2013 to 2021

Contact Info

Product

Resources

About