ReviewCell communication and signaling : CCS2026
The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.
Review in Cell communication and signaling : CCS, 2026. 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
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
2 citing papers in PubMed.
- Plant-Derived Senotherapeutics in Cellular Senescence: A Scoping Review of Preclinical Evidence, Mechanistic Pathways, and Metabolomic-Guided Discovery.International journal of molecular sciences · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The cGAS-STING pathway acts as a critical molecular hub connecting genomic instability with cellular senescence. Functioning as a key regulator of the innate immune system, this pathway detects aberrant cytoplasmic DNA to activate downstream inflammatory responses, thereby playing a pivotal role in aging-related diseases. This review systematically explores the core mechanisms by which the cGAS-STING pathway regulates cellular senescence, emphasizing its role in triggering senescence through the recognition of DNA damage signals (e.g., oxidative stress, telomere dysfunction) and promoting paracrine senescence effects via the production and release of the senescence-associated secretory phenotype (SASP). We focus on the crosstalk between this pathway and current research hotspots, including the hypoxic microenvironment, ammonia-induced cell death, neutrophil extracellular trap (NET) formation, and macrophage polarization, uncovering its intricate molecular network in cellular senescence regulation. Moreover, this review provides an in-depth analysis of the cGAS-STING pathway's pathological contributions and molecular mechanisms in aging-related diseases, along with a summary of potential therapeutic strategies targeting this pathway, based on recent advances. These findings provide a critical theoretical framework for understanding cellular senescence mechanisms and advancing anti-aging interventions.
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What Socratic 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 Socratic graph.