ArticleInternational journal of molecular sciences2021
Individual Expression of Hepatitis A Virus 3C Protease Induces Ferroptosis in Human Cells In Vitro.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Ferroptosis in liver diseases: molecular mechanisms, biomarker potential, and clinical translation.Frontiers in cell and developmental biology · 2026Review
- Recent progress in understanding ferroptosis mechanisms in infectious diseases.Frontiers in cellular and infection microbiology · 2026Review
- Synergetic contributions of Seneca Valley virus 3 C and 3D proteins to induction of ferroptosis for viral replication.Cellular and molecular life sciences : CMLS · 2025Article
- Limited impact of hepatitis A virus 3C protease-mediated cleavage on the functions of NEMO in human hepatocytes.Journal of virology · 2025Article
- Review
- Yeast-Based Screening of Anti-Viral Molecules.Microorganisms · 2024Review
- Expression and Purification of His-Tagged Variants of Human Hepatitis A Virus 3C Protease.Protein and peptide letters · 2024Article
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
- Article
- The Emerging Role of Ferroptosis in Various Chronic Liver Diseases: Opportunity or Challenge.Journal of inflammation research · 2023Review
- Viral-mediated activation and inhibition of programmed cell death.PLoS pathogens · 2022Review
- Ferroptosis in COVID-19-related liver injury: A potential mechanism and therapeutic target.Frontiers in cellular and infection microbiology · 2022Review
- The Emerging Role of Ferroptosis in Liver Diseases.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Regulated cell death (RCD) is a fundamental process common to nearly all living beings and essential for the development and tissue homeostasis in animals and humans. A wide range of molecules can induce RCD, including a number of viral proteolytic enzymes. To date, numerous data indicate that picornaviral 3C proteases can induce RCD. In most reported cases, these proteases induce classical caspase-dependent apoptosis. In contrast, the human hepatitis A virus 3C protease (3Cpro) has recently been shown to cause caspase-independent cell death accompanied by previously undescribed features. Here, we expressed 3Cpro in HEK293, HeLa, and A549 human cell lines to characterize 3Cpro-induced cell death morphologically and biochemically using flow cytometry and fluorescence microscopy. We found that dead cells demonstrated necrosis-like morphological changes including permeabilization of the plasma membrane, loss of mitochondrial potential, as well as mitochondria and nuclei swelling. Additionally, we showed that 3Cpro-induced cell death was efficiently blocked by ferroptosis inhibitors and was accompanied by intense lipid peroxidation. Taken together, these results indicate that 3Cpro induces ferroptosis upon its individual expression in human cells. This is the first demonstration that a proteolytic enzyme can induce ferroptosis, the recently discovered and actively studied type of RCD.
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