ArticleScience advances2025
Astrocytes-derived LCN2 triggers EV-A71-induced muscle soreness via accumulating lactate.
Article in Science advances, 2025. 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.
- Lactylation in influenza a virus infection: Current evidence, knowledge gaps, and future perspectives.Virulence · 2026Review
- Lcn2 Promotes Ferroptosis in Intracerebral Hemorrhage by Targeting Keap1 Tyr572 and Restricting Nrf2 Activation.MedComm · 2026Article
- Emerging roles of lipocalin-2-mediated neuroimmune interactions in chronic pain and itch.Frontiers in pharmacology · 2026Review
- The Role of Lactylation in Virus-Host Interactions.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral muscle soreness (VMS) is a common feature during acute viral infections, including those caused by enteroviruses, and it substantially diminishes patients' quality of life. At present, we aim to establish the "brain-muscle" axis to explore the underlying mechanisms of VMS. We initially observed that diminished pain threshold occurred in enterovirus A71 (EV-A71)-infected C57BL/6J and AG6 mice. Subsequently, RNA sequencing data showed that lipocalin 2 (LCN2) was up-regulated during multiple viral infections, including EV-A71, Japanese encephalitis virus, vesicular stomatitis virus, and West Nile virus, which all caused VMS. As expected,
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