ReviewJournal of biochemistry2025
Innate immune responses to lysosomal nucleic acid stress.
Review in Journal of biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- Multilayered interplay between the cGAS-STING pathway and autophagy.Autophagy reports · 2026Review
- Lysosomal checkpoints in renal autoimmunity: from antigen processing to metabolic-immune crosstalk.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleic acids (NAs) are recognized by endosomal Toll-like receptors (TLRs) and cytoplasmic sensors in innate immune cells. NAs accumulate within lysosomes due to either excessive NA influx or defective lysosomal degradation. The resultant storage of NAs and/or NA metabolites in the lysosome, referred to here as lysosomal NA stress, elicits a spectrum of responses, ranging from inflammation to tissue repair, through NA sensor activation. Although these responses contribute to host defence against infection, they may also drive diseases. For instance, loss of function of the lysosomal nucleoside transporter SLC29A3 drives lysosomal nucleoside stress, which activates TLR8 in macrophages to cause histiocytic diseases collectively called SLC29A3 disorders. Similarly, DNase II deficiency promotes lysosomal DNA stress, leading to activation of cytoplasmic double-stranded DNA sensors, such as cGAS-STING and AIM2, and thereby autoinflammatory and autoimmune diseases. Thus, lysosomal NA stress is viewed as a pivotal environmental signal that initiates innate immune responses.
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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 OpenQuestion graph.