ArticleFrontiers in biology2014
Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses.
Article in Frontiers in biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Herpesvirus Regulation of Selective Autophagy.Viruses · 2021Review
- Mitochondrial DNA copy number in cervical exfoliated cells and risk of cervical cancer among HPV-positive women.BMC women's health · 2020Article
- HTLV-1 basic leucine zipper factor protects cells from oxidative stress by upregulating expression of Heme Oxygenase I.PLoS pathogens · 2019Article
- Luteolin-7-Frontiers in microbiology · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Between 15-20% of human cancers are associated with infection by oncogenic viruses. Oncogenic viruses, including HPV, HBV, HCV and HTLV-1, target mitochondria to influence cell proliferation and survival. Oncogenic viral gene products also trigger the production of reactive oxygen species which can elicit oxidative DNA damage and potentiate oncogenic host signaling pathways. Viral oncogenes may also subvert mitochondria quality control mechanisms such as mitophagy and metabolic adaptation pathways to promote virus replication. Here, we will review recent progress on viral regulation of mitophagy and metabolic adaptation and their roles in viral oncogenesis.
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