Acyl-Coenzyme A Synthetase Long-Chain Family Member 4 Is Involved in Viral Replication Organelle Formation and Facilitates Virus Replication via Ferroptosis

Kung, Yu-An; Chiang, Hou‐Yu; Li, Meiling; Gong, Yu-Nong; Chiu, Hsiu‐Hui; Hung, Cheng‐Chieh; Huang, Po-Jung; Huang, San Yuan; Wang, Peiyu; Hsu, Tsu‐An; Brewer, Gary; Shih, Shin‐Ru

doi:10.1128/mbio.02717-21

Cited by 65 publications

(42 citation statements)

References 45 publications

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“…Those authors used several inhibitors targeting the cell cycle and the endocytosis pathway and showed that both are critical for coronavirus infection. Kung et al ( 170 ) found that ACSL4-mediated ferroptosis is required for HCoV-229E infection. They identified host factors using CRISPR loss-of-function screening with coxsackievirus A6.…”

Section: High-throughput Screening Identification Of Host Cell Factor...mentioning

confidence: 99%

Molecular Virology of SARS-CoV-2 and Related Coronaviruses

Kung

Lee

Chiang

et al. 2022

Microbiol Mol Biol Rev

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Section: High-throughput Screening Identification Of Host Cell Factor...mentioning

confidence: 99%

Molecular Virology of SARS-CoV-2 and Related Coronaviruses

Kung

Lee

Chiang

et al. 2022

Microbiol Mol Biol Rev

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“…( Yao Y. et al, 2021 ). (B) During SARs-Cov-2 infection, the Gpx4 mRNA level was decreased ( Wang et al, 2021a ) and iron overload was observed ( Zhou C. et al, 2020 ), and the induction of ferroptosis by SARS-Cov-2 could be rescued by ASCL4 inhibitors ( Kung et al, 2022 )…”

Section: Mechanism Of Ferroptosismentioning

confidence: 99%

“…What’s more, lipid metabolism is involved in viral replication by regulation of the formation, assembly, and release of replicative organelles. ASCL4, a key factor involved in lipid metabolism and ferroptosis, greatly promoted the replication of some enteroviruses and coronaviruses ( Kung et al, 2022 ). In ASCL4 knockout cells, the viral titers of enteroviruses such as CV-A6, coronaviruses such as Cov-229E, influenza virus (IAV), and Zika virus were lower than those in the normal cells.…”

Section: Mechanism Of Ferroptosismentioning

confidence: 99%

“…Ferroptosis inhibitors includes iron chelators, like the famous one DFO (deferoxamine), has been approved by the FDA for the treatment of iron overload ( Meyer, 2006 ). Meanwhile, the induction of ferroptosis by SARS-Cov-2 could be rescued by ASCL4 inhibitors ( Kung et al, 2022 ). Also, SARS-Cov-2 showed inhibitory effects on the expression of the selenoprotein GPX4 mRNA level in vivo ( Wang et al, 2021a ).…”

Section: Mechanism Of Ferroptosismentioning

confidence: 99%

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Ferroptosis: A mixed blessing for infectious diseases

et al. 2022

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To date, it has been confirmed that the occurrence and development of infectious diseases are tightly associated with regulatory cell death processes, such as apoptosis, autophagy, and necroptosis. Ferroptosis, as a newly discovered form of regulatory cell death characterized by iron-dependent lipid peroxidation, is not only closely associated with tumor progression, but is also found to be tightly related to the regulation of infectious diseases, such as Tuberculosis, Cryptococcal meningitis, Malaria and COVID-2019. The emerging critical roles of ferroptosis that has been found in infectious disease highlight ferroptosis as a potential therapeutic target in this field, which is therefore widely expected to be developed into new therapy strategy against infectious diseases. Here, we summarized the underlying mechanisms of ferroptosis and highlighted the intersections between host immunity and ferroptosis. Moreover, we illuminated the roles of ferroptosis in the occurrence and progression of different infectious diseases, which might provide some unique inspiration and thought-provoking perspectives for the future research of these infectious diseases, especially for the development of ferroptosis-based therapy strategy against infectious diseases.

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“…Enteroviruses can induce ferroptosis through ACSL4. However, its inhibitors can reduce enteroviral yields ( 81 ).…”

Section: Viral Myocarditis and Ferroptosismentioning

confidence: 99%

Advances in cell death mechanisms involved in viral myocarditis

Yang

You

et al. 2022

Front. Cardiovasc. Med.

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Viral myocarditis is an acute inflammatory disease of the myocardium. Although many etiopathogenic factors exist, coxsackievirus B3 is a the leading cause of viral myocarditis. Abnormal cardiomyocyte death is the underlying problem for most cardiovascular diseases and fatalities. Various types of cell death occur and are regulated to varying degrees. In this review, we discuss the different cell death mechanisms in viral myocarditis and the potential interactions between them. We also explore the role and mechanism of cardiomyocyte death with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Exploring the mechanisms may help in the early identification and the development of effective treatments, thus improving the quality of life of patients with viral myocarditis. We believe that the inhibition of cardiomyocyte death has immense therapeutic potential in increasing the longevity and health of the heart.

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Acyl-Coenzyme A Synthetase Long-Chain Family Member 4 Is Involved in Viral Replication Organelle Formation and Facilitates Virus Replication via Ferroptosis

Cited by 65 publications

References 45 publications

Molecular Virology of SARS-CoV-2 and Related Coronaviruses

Molecular Virology of SARS-CoV-2 and Related Coronaviruses

Ferroptosis: A mixed blessing for infectious diseases

Advances in cell death mechanisms involved in viral myocarditis

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