Ferroptotic Cell Death: New Regulatory Mechanisms for Metabolic Diseases

Le, Yifei; Zhang, Zhijie; Wang, Cui; Lu, Dezhao

doi:10.2174/1871530320666200731175328

Cited by 20 publications

(17 citation statements)

References 150 publications

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“…Therefore, membrane lipid peroxidation caused by ferroptosis can damage cytomembranes and promote inflammatory reactions in cells. Dysregulation of ferroptosis has been reported in multiple physiological and pathological processes, such as cancer and metabolic diseases ( 155 , 156 ). In addition, studies have reported that ferroptosis plays a positive role in inflammation through immunogenicity ( 157 ).…”

Section: Pkm2: a Potential Promotor Of Proinflammatory Non-apoptotic-regulated Cell Deathmentioning

confidence: 99%

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Liu

Chen

et al. 2021

Front. Immunol.

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The cytokine storm is a marker of severity of various diseases and increased mortality. The altered metabolic profile and energy generation of immune cells affects their activation, exacerbating the cytokine storm. Currently, the emerging field of immunometabolism has highlighted the importance of specific metabolic pathways in immune regulation. The glycolytic enzyme pyruvate kinase M2 (PKM2) is a key regulator of immunometabolism and bridges metabolic and inflammatory dysfunction. This enzyme changes its conformation thus walks in different fields including metabolism and inflammation and associates with various transcription factors. This review summarizes the vital role of PKM2 in mediating immunometabolic reprogramming and its role in inducing cytokine storm, with a focus on providing references for further understanding of its pathological functions and for proposing new targets for the treatment of related diseases.

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Section: Pkm2: a Potential Promotor Of Proinflammatory Non-apoptotic-regulated Cell Deathmentioning

confidence: 99%

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Liu

Chen

et al. 2021

Front. Immunol.

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“…Iron, an essential trace element for humans and a necessary substance for life, plays a vital role in many biochemical processes, including oxygen transport, enzymatic reactions, and immune reactions. With accumulating research, various physiological and pathological processes, such as tumor, Parkinson's disease, atherosclerosis, viral infection, osteoporosis, immune response, and ischemia-reperfusion injury, have been found to be related to ferroptosis [ 6 – 8 ], and ferroptosis is expected to become a new research direction for disease treatment.…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis: A New Regulatory Mechanism in Osteoporosis

Liu

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Osteoporosis can be caused by a multitude of factors and is defined by a decrease in bone density and mass caused by the destruction of bone microstructure, resulting in increased bone brittleness. Thus, it is a systemic bone disease in which patients are prone to fracture. The role of ferroptosis in the pathogenesis of osteoporosis has become a topic of growing interest. In this review, we discuss the cell morphology, basic mechanisms of ferroptosis, the relationship between ferroptosis and osteoclasts and osteoblasts, as well as the relationship between ferroptosis and diabetic osteoporosis, steroid-induced osteoporosis, and postmenopausal osteoporosis. Emerging biomedical research has provided new insights into the roles of ferroptosis and osteoporosis, such as in cellular function, signaling pathways, drug inhibition, and gene silencing. The pathophysiology and mechanism of ferroptosis and osteoporosis need to be further studied and elucidated to broaden our understanding of iron metabolism and immune regulation. Studies using animal models of osteoporosis in vivo and cell models in vitro will help clarify the relationship between ferroptosis and osteoporosis and provide research ideas for the elucidation of new mechanisms and development of new technologies and new drugs for the treatment of osteoporosis in the future.

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“…Numerous studies have shown that this mode of death is closely related to various diseases, including nervous system diseases, tumors, ischemiareperfusion injury diseases, as well as kidney injury and iron metabolism diseases (17). Recently, an increasing number of studies have found that ferroptosis is involved in the pathogenesis of NASH (18). Tsurusaki et al [2019] demonstrated that hepatic ferroptosis inhibition protected NASH by suppressing the subsequent infiltration of immune cells and inflammatory reaction (19).…”

Section: Introductionmentioning

confidence: 99%

ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevation of GPX4 expression and lipid accumulation

Lü¹,

Qing²,

Yang³

et al. 2021

Ann Transl Med

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Background: ENO3 expression is upregulated in Non-alcoholic fatty liver disease (NAFLD) patient tissues, demonstrated that ENO3 might play crucial roles in NAFLD. However, the mechanism of ENO3 in NAFLD remains unclear. Therefore, this study aimed to investigate the regulatory mechanism of ENO3 in the progression of non-alcoholic steatohepatitis (NASH) in vivo and vitro NASH model. Methods: In vivo and vitro NASH model were established by methionine-choline deficient (MCD)-diet feeding and high free fatty acid (HFFA) induction in L02 cells. Loss and gain function of ENO3 and GPX4 was performed to study the mechanism in NASH. Western blot was used to detect the expression of ENO3 and GPX4. Hematoxylin and eosin (H&E), picrosirius Red and Oil Red O staining was used to evaluate histopathology of liver in NASH model. Ferroptosis indicators were measured by assay kits according to the manufacturer's instructions.Results: NASH mouse model was successfully established induced by MCD diet with steatosis, inflammatory infiltration, ballooning and fibrosis observed in the liver tissue. The expression of ENO3 and GPX4 was significantly elevated while ferroptosis was inhibited in NASH mice and cell model. Upregulation of both ENO3 and GPX4 could promote the lipid accumulation in L02 cells. In addition, overexpressed ENO3 attenuated the status of ferroptosis.Conclusions: In the present study, we demonstrate that ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for NASH.

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Ferroptotic Cell Death: New Regulatory Mechanisms for Metabolic Diseases

Cited by 20 publications

References 150 publications

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Role of PKM2-Mediated Immunometabolic Reprogramming on Development of Cytokine Storm

Ferroptosis: A New Regulatory Mechanism in Osteoporosis

ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevation of GPX4 expression and lipid accumulation

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