ReviewJACC. Asia2025
The CGAS-STING1 Pathway as a Mediator of Innate Immune Response in Cardiovascular Disease.
Review in JACC. Asia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Understanding cardiovascular aging as a disorder of mitochondrial network.The journal of cardiovascular aging · 2026Article
- Activation of the cGAS-STING Pathway by NETs Promotes Inflammatory Injury in Myocardial Ischemia-Reperfusion.Journal of inflammation research · 2026Article
- Humanized hiPSC Platforms for I/R Injury: Advancing Toward Precision Cardioprotection.Cardiovascular therapeutics · 2026Review
- Self-DNA by Activating the CGAS-STING1 Pathway Contributes to the Pathogenesis of Atherosclerosis.Current atherosclerosis reports · 2025Review
- Cardiomyocyte cytosolic nuclear self-DNA contributes to the pathogenesis of desmoplakin cardiomyopathy.JCI insight · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The innate immune response, a rapid and cell-autonomous response of the cell to the pathogens, recognizes the external as well as the internal pathogens, such as self-DNA, released from the damaged cells. The response activates a set of molecules that induce the expression of proinflammatory cytokines and chemokines and leads to inflammation, fibrosis, and cell death. The innate immune response comprised of DNA-sensing protein cyclic guanosine monophosphate-adenosine monophosphate synthase (CGAS) and its downstream molecules, the stimulator of interferon genes 1 (STING1), TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and nuclear factor kappa B (NFκB), are activated in several cardiovascular diseases, including hereditary cardiomyopathies, myocardial infarction, hypertension, atherosclerosis, and aortic aneurysm. The genetic deletion of key molecules in this pathway, such as CGAS, STING1, and interferon regulatory factor 3, affords salubrious effects, including improving survival and cardiac dysfunction, rendering the CGAS-STING1 pathway an attractive therapeutic target in cardiovascular disease.
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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.