ArticleCell death & disease2018
The cytotoxicity of coxsackievirus B3 is associated with a blockage of autophagic flux mediated by reduced syntaxin 17 expression.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- 3C suppresses PINK1-mediated mitophagy and contributes to coxsackievirus B3 replication.Virulence · 2026Article
- The molecular mechanisms of autophagy-virus interactions: from antiviral defense to viral counterstrategies.FEMS microbiology reviews · 2026Review
- Cellular protein quality control in viral myocarditis: molecular mechanisms and therapeutic implication.Microbiology and molecular biology reviews : MMBR · 2025Review
- Rapid Screening to Identify Antivirals against Persistent and Acute Coxsackievirus B3 Infection.ACS infectious diseases · 2024Article
- Neurotropic virus infection and neurodegenerative diseases: Potential roles of autophagy pathway.CNS neuroscience & therapeutics · 2024Review
- Exacerbation of atherosclerosis by STX17 knockdown: Unravelling the role of autophagy and inflammation.Journal of cellular and molecular medicine · 2024Article
- Regulation of Autophagosome-Lysosome Fusion by Human Viral Infections.Pathogens (Basel, Switzerland) · 2024Review
- The relationship between autophagy and respiratory viruses.Archives of microbiology · 2024Review
- Mitochondrial extracellular vesicles, autoimmunity and myocarditis.Frontiers in immunology · 2024Review
- Parkin plays a crucial role in acute viral myocarditis by regulating mitophagy activity.Theranostics · 2024Article
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- Echovirus induces autophagy to promote viral replicationFrontiers in immunology · 2023Article
- TBK1 and GABARAP family members suppress Coxsackievirus B infection by limiting viral production and promoting autophagic degradation of viral extracellular vesicles.PLoS pathogens · 2022Article
- The encephalomyocarditis virus Leader promotes the release of virions inside extracellular vesicles via the induction of secretory autophagy.Nature communications · 2022Article
- SARS-CoV-2: A Master of Immune Evasion.Biomedicines · 2022Review
- Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.iScience · 2022Article
- Novel Antiviral Activity of Ethyl 3-Hydroxyhexanoate Against Coxsackievirus B Infection.Frontiers in microbiology · 2022Article
- Mechanisms and Therapeutic Strategies of Viral Myocarditis Targeting Autophagy.Frontiers in pharmacology · 2022Review
- Circular RNA circ_0076631 promotes coxsackievirus B3 infection through modulating viral translation by sponging miR-214-3p.Frontiers in microbiology · 2022Article
- The interplay between emerging human coronavirus infections and autophagy.Emerging microbes & infections · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coxsackievirus B3 (CVB3) is an important human pathogen linked to cardiac arrhythmias and acute heart failure. CVB3 infection has been reported to induce the formation of autophagosomes that support the viral replication in host cells. Interestingly, our study shows that the accumulation of autophagosomes during CVB3 infection is caused by a blockage of autophagosome-lysosome fusion rather than the induction of autophagosome biogenesis. Moreover, CVB3 decreases the transcription and translation of syntaxin 17 (STX17), a SNARE (soluble N-ethylmaleimide-sensitive factor activating protein receptor) protein involved in autophagosome-lysosome fusion. Overexpression of STX17 restored the autophagic flux, alleviated the virus-induced lysosomal dysfunction, and decreased the apoptosis induced by CVB3 infection in HeLa cells. Taken together, our results suggest that CVB3 infection impairs the autophagic flux by blocking autophagosome-lysosome fusion. These findings thus point to potential new therapeutic strategies targeting STX17 or autophagosome-lysosome fusion for treating CVB3-associated diseases.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.