Authors
Shiqing Tan, Eugenie Nepovimova, Marian Valko, Klaudia Jomova, Qinghua Wu, Kamil Kuca
Published in
Cell communication and signaling : CCS. Volume 24. Issue 1. Apr 01, 2026. Epub Apr 01, 2026.
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.
PMID:
41923153
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.
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