Advances in cell death mechanisms involved in viral myocarditis

Yang, Yang; Li, Wang; You, Benshuai; Zhou, Chenglin

doi:10.3389/fcvm.2022.968752

Cited by 4 publications

(3 citation statements)

References 126 publications

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“…NCOA4 overexpression enhances FER degradation and leads to iron release. Iron converts the LOOH into hydroxyl radicals via the Fenton reaction, ultimately inducing ferroptosis and promoting cell damage [ 95 ]. Transferrin receptor-1 (TfR-1) can facilitate the entrance of iron held by transferrin into the cells [ 87 ].…”

Section: Ferroptosis and Covid-19mentioning

confidence: 99%

“…It has also been considered the primary determinant for dictating ferroptosis sensitivity and reshaping cellular lipid composition [ 97 ]. The virus suppresses mRNA expression of ferroptosis-associated GPx4, DNA synthesis-related TrxR, and endoplasmic reticulum selenoproteins [ 95 ]. Due to the lack of GPx4, GSH cannot be peroxidized to reduce the ROS of lipids formed in the Fenton reaction.…”

Section: Ferroptosis and Covid-19mentioning

confidence: 99%

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Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

et al. 2023

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Ferroptosis is a recently discovered form of programmed cell death. It is characterized by the accumulation of iron and lipid hydroperoxides in cells. Vitamin K is known to have antioxidant properties and plays a role in reducing oxidative stress, particularly in lipid cell membranes. Vitamin K reduces the level of reactive oxygen species by modulating the expression of antioxidant enzymes. Additionally, vitamin K decreases inflammation and potentially prevents ferroptosis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection leading to coronavirus disease 2019 (COVID-19) is associated with oxidant–antioxidant imbalance. Studies have shown that intensified ferroptosis occurs in various tissues and cells affected by COVID-19. Vitamin K supplementation during SARS-CoV-2 infection may have a positive effect on reducing the severity of the disease. Preliminary research suggests that vitamin K may reduce lipid peroxidation and inhibit ferroptosis, potentially contributing to its therapeutic effects in COVID-19 patients. The links between ferroptosis, vitamin K, and SARS-CoV-2 infection require further investigation, particularly in the context of developing potential treatment strategies for COVID-19.

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Section: Ferroptosis and Covid-19mentioning

confidence: 99%

Section: Ferroptosis and Covid-19mentioning

confidence: 99%

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

et al. 2023

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“…Moreover, a variety of viruses have been identified to utilize TFR1 for binding and entry the host cells. CVB3 infection increased iron accumulation and TFRC expression, which subsequently aggravated the ferroptosis (Yang et al, 2022a;Yi et al, 2022). Certain viruses have been found to hijack cellular TFR1 and promote virus internalization and by clathrin-mediated endocytosis.…”

Section: Ferroptosis and Viral Infections Iron Regulation And Viral I...mentioning

confidence: 99%

The role of ferroptosis in virus infections

Wang,

Zhu,

Ren

et al. 2023

Front. Microbiol.

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Regulated cell death (RCD) is a strategy employed by host cells to defend invasions of pathogens, such as viruses and bacteria. Ferroptosis is a type of RCD characterized by excessive accumulation of iron and lipid peroxidation. While ferroptosis is primarily considered as a mechanism associated with tumorigenesis, emerging evidence begin to suggest that it may play essential role during virus infections. Recent studies illustrated that activation of ferroptosis could either induce or prohibit various types of RCDs to facilitate virus replication or evade host surveillance. More experimental evidence has demonstrated how viruses regulate ferroptosis to influence replication, transmission, and pathogenesis. This review summarizes ferroptosis-related metabolism, including iron metabolism, lipid peroxidation, and antioxidant metabolism. Furthermore, we discuss the interplay between viral infections and host ferroptosis process, with a focus on the mechanism of how viruses exploit ferroptosis for its own replication. Understanding how ferroptosis impacts virus infection can offer valuable insights into the development of effective therapeutic strategies to combat virus infections.

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Immunopathogenesis and immunomodulatory therapy for myocarditis

Zhou

et al. 2023

Sci. China Life Sci.

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Myocarditis is an inflammatory cardiac disease characterized by the destruction of myocardial cells, infiltration of interstitial inflammatory cells, and fibrosis, and is becoming a major public health concern. The aetiology of myocarditis continues to broaden as new pathogens and drugs emerge. The relationship between immune checkpoint inhibitors, severe acute respiratory syndrome coronavirus 2, vaccines against coronavirus disease-2019, and myocarditis has attracted increased attention. Immunopathological processes play an important role in the different phases of myocarditis, affecting disease occurrence, development, and prognosis. Excessive immune activation can induce severe myocardial injury and lead to fulminant myocarditis, whereas chronic inflammation can lead to cardiac remodelling and inflammatory dilated cardiomyopathy. The use of immunosuppressive treatments, particularly cytotoxic agents, for myocarditis, remains controversial. While reasonable and effective immunomodulatory therapy is the general trend. This review focuses on the current understanding of the aetiology and immunopathogenesis of myocarditis and offers new perspectives on immunomodulatory therapies.

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Advances in cell death mechanisms involved in viral myocarditis

Cited by 4 publications

References 126 publications

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

Links between Vitamin K, Ferroptosis and SARS-CoV-2 Infection

The role of ferroptosis in virus infections

Immunopathogenesis and immunomodulatory therapy for myocarditis

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