Inhibition of ferroptosis alleviates high-power microwave-induced myocardial injury

Wang, Yu; Lu, Yan; Chen, Wen; Xie, Xiaohua

doi:10.3389/fcvm.2023.1157752

Cited by 5 publications

(2 citation statements)

References 70 publications

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“…When examining cardiomyopathy, our investigation focused on several subtypes, namely Diabetic cardiomyopathy (DCM), Hypertrophic cardiomyopathy, post-transplant cardiomyopathy, Septic cardiomyopathy, Doxorubicin-induced cardiomyopathy (DIC), and radioactive cardiomyopathy [ 533 – 537 ]. The primary objective was to explore the association between the diverse spectrum of CVDs and ferroptosis, while also identifying potential novel compounds that target iron metabolism and ferroptosis within the context of CVDs (Tables 7 & 8 ).…”

Section: Ferroptosis In Pathologiesmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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Section: Ferroptosis In Pathologiesmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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“…It indicates that iron accumulation as well as oxidative stress were aggravated in the CCI model. In addition, Fer-1, a ferroptosis inhibitor, upregulates the expression of GPX4 and downregulates the expression of ACSL4 ( Wang et al, 2023 ). And in a related study, it was found that treatment with ferrostatin-1 significantly inhibited the onset of oxidative stress in brain tissue, improved the structure of brain tissue after hemorrhage, protected neurons, and promoted neurological function in recovery of rats.…”

Section: The Relationship Between Neuropathic Pain and Ferroptosismentioning

confidence: 99%

Ferroptosis: a new regulatory mechanism in neuropathic pain

Li,

Guo,

Gao

et al. 2023

Front. Aging Neurosci.

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Neuropathic pain (NP) is pain caused by damage to the somatosensory system. It is a common progressive neurodegenerative disease that usually presents with clinical features such as spontaneous pain, touch-evoked pain, nociceptive hyperalgesia, and sensory abnormalities. Due to the complexity of the mechanism, NP often persists. In addition to the traditionally recognized mechanisms of peripheral nerve damage and central sensitization, excessive iron accumulation, oxidative stress, neuronal inflammation, and lipid peroxidation damage are distinctive features of NP in pathophysiology. However, the mechanisms linking these pathological features to NP are not fully understood. The complexity of the pathogenesis of NP greatly limits the development of therapeutic approaches for NP. Ferroptosis is a novel form of cell death discovered in recent years, in which cell death is usually accompanied by massive iron accumulation and lipid peroxidation. Ferroptosis-inducing factors can affect glutathione peroxidase directly or indirectly through different pathways, leading to decreased antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. It has been shown that ferroptosis is closely related to the pathophysiological process of many neurological disorders such as NP. Possible mechanisms involved are changes in intracellular iron ion levels, alteration of glutamate excitability, and the onset of oxidative stress. However, the functional changes and specific molecular mechanisms of ferroptosis during this process still need to be further explored. How to intervene in the development of NP by regulating cellular ferroptosis has become a hot issue in etiological research and treatment. In this review, we systematically summarize the recent progress of ferroptosis research in NP, to provide a reference for further understanding of its pathogenesis and propose new targets for treatment.

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