Relieving ferroptosis may partially reverse neurodegeneration of the auditory cortex

Chen, Xi; Li, Dan; Sun, Haiying; Wang, Wenwen; Wu, Han; Kong, Wen; Kong, Weijia

doi:10.1111/febs.15266

Cited by 33 publications

(21 citation statements)

References 75 publications

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“…A recent study found that Tf and TfR1, mainly responsible for intestinal iron absorption, play the critical role in ferroptotic cell death [ 23 , 31 ]. Elevated plasma level of TfR1 increased the amount of intracellular iron, which might promote ferroptosis, e.g., leading to auditory cortex neurodegeneration [ 32 ]. The redundant intracellular iron is stored in ferritin which is composed of FTL and FTH1.…”

Section: Mechanisms Of Ferroptosismentioning

confidence: 99%

The Regulatory Effects and the Signaling Pathways of Natural Bioactive Compounds on Ferroptosis

Zhang

Geng

et al. 2021

Foods

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Natural bioactive compounds abundantly presented in foods and medicinal plants have recently received a remarkable attention because of their various biological activities and minimal toxicity. In recent years, many natural compounds appear to offer significant effects in the regulation of ferroptosis. Ferroptosis is the forefront of international scientific research which has been exponential growth since the term was coined. This type of regulated cell death is driven by iron-dependent phospholipid peroxidation. Recent studies have shown that numerous organ injuries and pathophysiological processes of many diseases are driven by ferroptosis, such as cancer, arteriosclerosis, neurodegenerative disease, diabetes, ischemia-reperfusion injury and acute renal failure. It is reported that the initiation and inhibition of ferroptosis plays a pivotal role in lipid peroxidation, organ damage, neurodegeneration and cancer growth and progression. Recently, many natural phytochemicals extracted from edible plants have been demonstrated to be novel ferroptosis regulators and have the potential to treat ferroptosis-related diseases. This review provides an updated overview on the role of natural bioactive compounds and the potential signaling pathways in the regulation of ferroptosis.

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Section: Mechanisms Of Ferroptosismentioning

confidence: 99%

The Regulatory Effects and the Signaling Pathways of Natural Bioactive Compounds on Ferroptosis

Zhang

Geng

et al. 2021

Foods

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“…In this process, iron accumulation ( Shang et al, 2020 ) and administration of iron-bound, rather than iron-free TF, promote erastin-induced ferroptosis ( Gao et al, 2015 ). On the contrary, using some iron chelators [e.g., DFP ( Wu et al, 2020 ), DFO ( Wu et al, 2018 ; Chen et al, 2020 ), and BPS ( Codenotti et al, 2018 )] may suppress ferroptosis and provide a potential therapeutic approach for diseases. In fact, there are some iron-chelating agents under clinical development for the treatment of cancers [for review see Brown et al (2020) ].…”

Section: Discovery and Mechanisms Of Ferroptosismentioning

confidence: 99%

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Shen

Lin

et al. 2020

Front. Cell Dev. Biol.

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Acute central nervous system (CNS) injuries, such as stroke, traumatic brain injury (TBI), and spinal cord injury (SCI) present a grave health care challenge worldwide due to high morbidity and mortality, as well as limited clinical therapeutic strategies. Established literature has shown that oxidative stress (OS), inflammation, excitotoxicity, and apoptosis play important roles in the pathophysiological processes of acute CNS injuries. Recently, there have been many studies on the topic of ferroptosis, a form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxidation. Some studies have revealed an emerging connection between acute CNS injuries and ferroptosis. Ferroptosis, induced by the abnormal metabolism of lipids, glutathione (GSH), and iron, can accelerate acute CNS injuries. However, pharmaceutical agents, such as iron chelators, ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1), can inhibit ferroptosis and may have neuroprotective effects after acute CNS injuries. However, the specific mechanisms underlying this connection has not yet been clearly elucidated. In this paper, we discuss the general mechanisms of ferroptosis and its role in stroke, TBI, and SCI. We also summarize ferroptosis-related drugs and highlight the potential therapeutic strategies in treating various acute CNS injuries. Additionally, this paper suggests a testable hypothesis that ferroptosis may be a novel direction for further research of acute CNS injuries by providing corresponding evidence.

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“…IRP2 is essential in regulating iron in the brain, and IRP2 dysregulation is closely related to iron accumulation in neurodegeneration [24, 28]. In the study of aging-related auditory cortical neurodegeneration, it has been found that the upregulation of IRP2 increases intracellular iron levels and causes ferroptosis [29].…”

Section: Related Mechanisms Of Ferroptosismentioning

confidence: 99%

Ferroptosis Is Regulated by Mitochondria in Neurodegenerative Diseases

et al. 2020

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Background: Neurodegenerative diseases are characterized by a gradual decline in motor and/or cognitive function caused by the selective degeneration and loss of neurons in the central nervous system, but their pathological mechanism is still unclear. Previous research has revealed that many forms of cell death, such as apoptosis and necrosis, occur in neurodegenerative diseases. Research in recent years has noticed that there is a new type of cell death in neurodegenerative diseases: ferroptosis. An increasing body of literature provides evidence for an involvement of ferroptosis in neurodegenerative diseases. Summary: In this article, we review a new form of cell death in neurodegenerative diseases: ferroptosis. Ferroptosis is defined as an iron-dependent form of regulated cell death, which occurs through the lethal accumulation of lipid-based reactive oxygen species when glutathione-dependent lipid peroxide repair systems are compromised. Several salient and established features of neurodegenerative diseases (including lipid peroxidation and iron dyshomeostasis) are consistent with ferroptosis, which means that ferroptosis may be involved in the progression of neurodegenerative diseases. In addition, as the center of energy metabolism in cells, mitochondria are also closely related to the regulation of iron homeostasis in the nervous system. At the same time, neurodegenerative diseases are often accompanied by degeneration of mitochondrial activity. Mitochondrial damage has been found to be involved in lipid peroxidation and iron dyshomeostasis in neurodegenerative diseases. Key Messages: Based on the summary of the related mechanisms of ferroptosis, we conclude that mitochondrial damage may affect neurodegenerative diseases by regulating many aspects of ferroptosis, including cell metabolism, iron dyshomeostasis, and lipid peroxidation.

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Relieving ferroptosis may partially reverse neurodegeneration of the auditory cortex

Cited by 33 publications

References 75 publications

The Regulatory Effects and the Signaling Pathways of Natural Bioactive Compounds on Ferroptosis

The Regulatory Effects and the Signaling Pathways of Natural Bioactive Compounds on Ferroptosis

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Ferroptosis Is Regulated by Mitochondria in Neurodegenerative Diseases

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