Interaction between macrophages and ferroptosis

Yang, Yan; Wang, Yu; Guo, Lin; Gao, Wen; Tang, Ting-Li; Yan, Miao

doi:10.1038/s41419-022-04775-z

Cited by 141 publications

(95 citation statements)

References 124 publications

(116 reference statements)

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“…Inhibitory factors existed in the microenvironment after SCI may affect endogenous stem cell differentiation [20], including astrocytes and microglia. Microglia are resident macrophages that normally remain static in the central nervous system [21]. After SCI, microglia and astrocytes are rapidly activated by various pathological factors.…”

Section: Discussionmentioning

confidence: 99%

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

Kan

Zhao

Liu

et al. 2022

Preprint

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Background: Spinal cord injury (SCI) is a type of trauma to the nervous system that can lead to severe dysfunction of the motor and sensory systems. The inhibitory microenvironment is the basis of secondary injury after SCI, and ferroptosis may aggravate secondary SCI. In this study, the role of ferroptosis inhibitor UAMC-3203 in the recovery of SCI was explored by examining the tissue structure, biochemical indexes, and motor function of rats after SCI. Methods: A model of SCI was established using Alice's method. The protective effect of UAMC-3203 on spinal cord neurons and the recovery of motor function were studied by Basso, Beattie, Bresnahan (BBB) score, incline plate test, Hematoxylin-eosin (HE) staining and Luxol Fast Blue (LFB) staining. Immunofluorescence and Elisa analysis were used to study the effect of UAMC-3203 on the microenvironment. Western blot analysis was used to measure the level of ferroptosis markers. Reactive oxygen species (ROS) and malondialdehyde (MDA) were detected to reflect the level of oxidation products. Results: We found that in the UAMC-3203 group, the loss and demyelination of neurons was reduced, the activation and proliferation of astrocytes and microglia and the secretion of related inflammatory cytokines was restrained, and motor function recovery was faster and better compared with those in the SCI group. Conclusions: UAMC-3203 has played an active role in the recovery process of SCI, providing evidence that post-SCI microenvironment imbalances are associated with ferroptosis.

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Section: Discussionmentioning

confidence: 99%

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

Kan

Zhao

Liu

et al. 2022

Preprint

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“…Iron load promotes the polarization of M1 macrophages and induces the release of inflammatory factors such as IL-6, IL-1β, TNF-α within M1 macrophages ( 60 ). The effect of ferroptosis on macrophage function is multifaceted, it can not only affect the polarization of macrophages, but also initiate the aggregation of macrophages ( 61 ).Ferroptosis is present in a variety of diseases, and the removal of ferroptosis cells is performed by macrophages. Damaged-associated molecular pattern molecules (DAMPs) can recruit and activate macrophages.…”

Section: Itaconate Inhibits Ferroptosis To Play a Role In Macrophage ...mentioning

confidence: 99%

Research Progress on the Mechanism of Itaconate Regulating Macrophage Immunometabolism

Shi

Cai²

2022

Front. Immunol.

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The field of immunology is undergoing rapid and dramatic changes. Immunometabolism, a change in metabolic pathways within immune cells, is a key determinant in the activation of immune cells, and intermediates of immunometabolic processes which can influence inflammatory gene expression and play a role in inflammation. Itaconate is one of the most representative metabolites, produced in the tricarboxylic acid cycle (TCA cycle), which links macrophage metabolism, oxidative stress response and immune response to regulate macrophage activity, playing an important role in the function of macrophages. In this paper, we review the mechanisms of the metabolite itaconate and its derivatives in the regulation of macrophage immune metabolism, intending to gain further insight into the role and mechanisms of this metabolite in macrophages and provide new ideas for the mechanisms and treatment of clinical diseases.

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“…Free iron accelerates this modification process through the action of hydroxyl free radicals. Monocytes adhere to the vascular endothelium and are transferred to the subendothelium through chemotaxis to transform into macrophages (66). Macrophages serve a pivotal role in AS progression, recognizing and destroying endothelial cells.…”

Section: Ferroptosis Is Involved In the Formation And Progression Of Asmentioning

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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Interaction between macrophages and ferroptosis

Cited by 141 publications

References 124 publications

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

UAMC-3203 improves the inhibitory microenvironment to repair spinal cord injury by inhibiting ferroptosis

Research Progress on the Mechanism of Itaconate Regulating Macrophage Immunometabolism

Potential intervention target of atherosclerosis: Ferroptosis (Review)

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