ArticleBMC pharmacology & toxicology2023
GAS-STING signaling plays an essential pathogenetic role in Doxorubicin-Induced Cardiotoxicity.
Article in BMC pharmacology & toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 10 citations in OpenAlex.
- The Therapeutic Potential of Stem Cell Therapy for Doxorubicin-Induced Cardiotoxicity: A Narrative Review.Health science reports · 2026Article
- Emerging roles of the cGAS/STING pathway in cardiovascular diseases.The Journal of clinical investigation · 2026Review
- Comparative Analysis of Doxorubicin-Induced Cardiotoxicity in Tumor-Bearing and Non-Tumor-Bearing Mouse Models: A Transcriptomic Methodological Study.International journal of molecular sciences · 2026Article
- Integrated multi-omics reveals acylcarnitine accumulation as an early driver of doxorubicin-induced cardiotoxicity targeted by chlorogenic acid.Frontiers in pharmacology · 2026Article
- Review
- Mitochondrial Amount Determines Doxorubicin-Induced Cardiotoxicity in Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiomyocyte GSDME Drives Doxorubicin-Induced Cardiotoxicity by Targeting the CCL2-CCR2 Axis.International journal of biological sciences · 2025Article
- cGAS/STING signalling pathway in senescence and oncogenesis.Seminars in cancer biology · 2024Review
- NOX4 aggravates doxorubicin-induced cardiomyocyte pyroptosis by increasing reactive oxygen species content and activating the NLRP3 inflammasome.Cardiovascular diagnosis and therapy · 2024Article
- The cGAS-STING/PERK-eIF2α: Individual or Potentially Collaborative Signaling Transduction in Cardiovascular Diseases.International journal of biological sciences · 2024Review
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe severe unfavorable effects of doxorubicin on the heart restrict its clinical usage. Numerous investigations document that cyclic GMP-AMP synthase (cGAS) activator of interferon genes (STING) cascade influences inflammation along with the immune response in a variety of diseases. The pathophysiological function of the cGAS-STING cascade in Doxorubicin-induced cardiomyopathy (DIC) is, nevertheless, unknown.
methodsIn vivo, cardiotoxicity was triggered by a single dose of intra-peritoneal inoculation of doxorubicin (15 mg/kg) in wild-type C57BL/6J mice and STING knockdown animals. Adeno-associated virus 9 (AAV9) was utilized to silence STING. qPCR along with Western blotting were adopted to assess alterations in the cGAS/STING cascade. To assess cardiac function, we employed echocardiography coupled with histology, as well as molecular phenotyping. In vitro, HL-1 cardiomyocytes were introduced as test models.
resultsIn wild type mice, doxorubicin stimulation significantly activated the cGAS/STING pathway. STING silencing increased rate of survival along with heart function in mice, as well as diminished myocardial inflammatory cytokines along with apoptosis. These observations were also confirmed by utilizing siRNA of STING in vitro studies.
conclusionThis research premise established that STING inhibition could alleviate Dox-triggered cardiotoxicity in mice. As a result, preventing DIC by repressing STING in cardiomyocytes might be a possible treatment approach.
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