ArticleFrontiers in immunology2025
The role of gasdermin-mediated mitochondrial RNA release in amplifying secondary immune response during microbial infection.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Mitochondrial RNA-Type I Interferon Axis in Sjögren's Disease: Molecular Mechanisms and Translational Implications.International journal of molecular sciences · 2026Review
- Interferon-alpha selectively signals mitochondrial pore opening to allow mitochondrial RNA release in systemic lupus erythematosus: pathophysiological implications.Cell communication and signaling : CCS · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytoplasmic RNA serves as a typical damage-associated molecular pattern (DAMP) signal; yet the mechanisms governing its release and role in inflammatory tissue damage remain poorly understood. In our study, we demonstrated that mimicking bacterial infection by lipopolysaccharide (LPS) combined with Nigericin (Ng) effectively activates Gasdermin D (GSDMD). Conversely, Vesicular Stomatitis Virus (VSV) selectively activates Gasdermin E (GSDME). Both GSDMD and GSDME form pores in the mitochondrial membrane, facilitating the release of mitochondrial RNA (mtRNA) into the cytosol. This released mtRNA is recognized by the RNA sensor Viral Interferon Stimulated Gene Activator (VISA), which subsequently induces a robust secondary inflammatory response. Importantly, the inhibition of GSDMD and GSDME prevents mitochondrial dysfunction and mtRNA release, thereby attenuating secondary inflammatory response mediated by the VISA pathway. Utilizing an experimental mice model, we found that LPS-induced lung tissue inflammation was restored by VISA knockout (VISA
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