ReviewCell2021
Cytoplasmic DNA: sources, sensing, and role in aging and disease.
Review in Cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 1 of them a synthesis that pooled it.
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
186 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.
- cGAS in nucleus: The link between immune response and DNA damage repair.Frontiers in immunology · 2022Pooled it
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- TREX1 limits anti-tumor immunity by degrading short cytosolic DNA molecules.EMBO reports · 2026Article
- The role of cytosolic mitochondrial DNA as a mitochondrial danger signal for stromal fibroblasts in forming the tumor-promoting microenvironment following radiation exposure.Journal of radiation research · 2026Review
- The Hallmarks of Aging: From Molecular Mechanisms to Clinical Translation.International journal of molecular sciences · 2026Review
- Article
- Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging.Nature aging · 2026Article
- Leaky oocytes propagate cGAS-STING signaling.Nature aging · 2026Article
- cGAS-deficient mice display premature aging associated with derepression of LINE1 elements and inflammation.Nature aging · 2026Article
- Loss of cGAS disrupts H3K9me3 organization and derepresses LINE1 to cause inflammaging.Nature aging · 2026Article
- MUTYH Activity Maintains Telomere Stability in Response to Chronic Telomeric 8-Oxoguanine Damage in Cancer Cells.Biomolecules · 2026Article
- TRF2 enriched cytoplasmic chromatin drives cGAS-STAT1-mediated inflammation in senescence.iScience · 2026Article
- MDM2 binds and suppresses RNA polymerase III to restrain the innate immune response to cytosolic DNA.Cell death and differentiation · 2026Article
- cGAS-STING signaling in aging and age-related diseases: therapeutic promise and precaution.Archives of pharmacal research · 2026Review
- Dataset of RNA-seq profiles from THP-1-derived macrophages pretreated with AZD7648 and stimulated with CT DNA.Data in brief · 2026Article
- PLIN2-PGAM5-regulated lipid droplet-mitochondria contacts drive microglial neuroinflammation after spinal cord injury via fatty acid metabolic reprogramming.Cell death and differentiation · 2026Article
- DNA Sensing and Neuroinflammation: Mechanistic Insights into cGAS-STING Biology and Therapeutic Translation in Age-Related Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Discovery of MK-2118, a Small-Molecule Agonist of STING.ACS medicinal chemistry letters · 2026Article
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
- Activating the vagus nerve-adrenal anti-inflammatory axis to delay aging: A randomized controlled trial protocol.Contemporary clinical trials communications · 2026Article
126 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Endogenous cytoplasmic DNA (cytoDNA) species are emerging as key mediators of inflammation in diverse physiological and pathological contexts. Although the role of endogenous cytoDNA in innate immune activation is well established, the cytoDNA species themselves are often poorly characterized and difficult to distinguish, and their mechanisms of formation, scope of function and contribution to disease are incompletely understood. Here, we summarize current knowledge in this rapidly progressing field with emphases on similarities and differences between distinct cytoDNAs, their underlying molecular mechanisms of formation and function, interactions between cytoDNA pathways, and therapeutic opportunities in the treatment of age-associated diseases.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.