ArticleCirculation2018
Cytosolic DNA Sensing Promotes Macrophage Transformation and Governs Myocardial Ischemic Injury.
Article in Circulation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.
What it found
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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.
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Who cites it
163 citing papers in PubMed, 259 citations in OpenAlex.
- U-shaped association between plasma cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) levels and myocardial infarction.BMC cardiovascular disorders · 2025Trial
- Artificial platelets suppressing deep vein thrombosis via competitive adhesion.Bioactive materials · 2026Article
- Mitochondrial Quality Control Links Exercise to Sterile Inflammation in the Cardiovascular System: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Macrophage USP7 aggravates acute myocardial infarction by inhibiting STING degradation through the ESCRT pathway.Cell death and differentiation · 2026Article
- ATP6AP2 ameliorates inflammation and pyroptosis in heart failure by promoting lysosome-dependent STING degradation.Apoptosis : an international journal on programmed cell death · 2026Article
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Carfilzomib Induces Cardiotoxicity by Blocking Autophagic Flux Through the cGAS-STING Signaling Pathway.Biomolecules · 2026Article
- Macrophage-specific circular RNA circHIPK2, inflammation, and fibrosis after myocardial infarction.European heart journal · 2026Article
- PARKIN overexpression confers cardioprotection via suppressing the mtDNA-cGAS-STING axis in myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- Review
- VCAM-1/Ezrin axis antagonizes myocardial damage in ischemia-reperfusion injury.Cell death and differentiation · 2026Article
- Nonlinear Bivariate Associations and Mononuclear Cell-Type-Specific Expression Level Differences in the STING Signalling Pathway.Journal of cellular and molecular medicine · 2026Article
- Prussian blue nanoparticles targeting multiple PANoptosome-mediated PANoptosis for myocardial ischemia-reperfusion injury therapy.Nature communications · 2026Article
- Chronic and non-canonical cGAS-STING activation: implications for health, disease, cancer, and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Targeting age-related LINE-1 activation alleviates cardiac aging.Nature aging · 2026Article
- M2 macrophage exosomes reverse heart failure post-myocardial infarction by suppressing type 1 interferon signaling in myeloid cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Astrocytic SIRT3 Alleviates Neuroinflammatory Responses After Cerebral Ischemia/reperfusion by Inhibiting the cGAS-STING Pathway.Inflammation · 2026Article
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- Periodontitis and cardiovascular diseases: bridging the gap through mitochondrial dysfunction.Frontiers in oral health · 2026Review
103 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMyocardium irreversibly injured by ischemic stress must be efficiently repaired to maintain tissue integrity and contractile performance. Macrophages play critical roles in this process. These cells transform across a spectrum of phenotypes to accomplish diverse functions ranging from mediating the initial inflammatory responses that clear damaged tissue to subsequent reparative functions that help rebuild replacement tissue. Although macrophage transformation is crucial to myocardial repair, events governing this transformation are poorly understood.
methodsHere, we set out to determine whether innate immune responses triggered by cytoplasmic DNA play a role.
resultsWe report that ischemic myocardial injury, along with the resulting release of nucleic acids, activates the recently described cyclic GMP-AMP synthase-stimulator of interferon genes pathway. Animals lacking cyclic GMP-AMP synthase display significantly improved early survival after myocardial infarction and diminished pathological remodeling, including ventricular rupture, enhanced angiogenesis, and preserved ventricular contractile function. Furthermore, cyclic GMP-AMP synthase loss of function abolishes the induction of key inflammatory programs such as inducible nitric oxide synthase and promotes the transformation of macrophages to a reparative phenotype, which results in enhanced repair and improved hemodynamic performance.
conclusionsThese results reveal, for the first time, that the cytosolic DNA receptor cyclic GMP-AMP synthase functions during cardiac ischemia as a pattern recognition receptor in the sterile immune response. Furthermore, we report that this pathway governs macrophage transformation, thereby regulating postinjury cardiac repair. Because modulators of this pathway are currently in clinical use, our findings raise the prospect of new treatment options to combat ischemic heart disease and its progression to heart failure.
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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.