ArticlePloS one2015
Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Tranexamic acid inhibits mitochondrial DNA release and reduces inflammatory response in an in vitro model of OGD/R-induced Caco-2 cell injury.BMC pharmacology & toxicology · 2026Article
- The central role of mitochondrial pathology in sepsis-induced cardiomyopathy: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Advances in mitochondria-nucleus crosstalk in septic cardiomyopathy.Cell biology and toxicology · 2025Review
- Klotho: A multifaceted protector in sepsis-induced organ damage and a potential therapeutic target.World journal of critical care medicine · 2025Review
- Myocardial pyruvate dehydrogenase kinase 4 drives sex-specific cardiac responses to endotoxemia.JCI insight · 2025Article
- Nrf2 Signaling Pathway: Focus on Oxidative Stress in Spinal Cord Injury.Molecular neurobiology · 2025Review
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Regulation of mitochondrial autophagy by lncRNA MALAT1 in sepsis-induced myocardial injury.European journal of medical research · 2024Article
- Mitochondrial dysfunction in sepsis: mechanisms and therapeutic perspectives.Critical care (London, England) · 2024Review
- Therapeutic Strategies Targeting Mitochondrial Dysfunction in Sepsis-induced Cardiomyopathy.Cardiovascular drugs and therapy · 2024Review
- Alleviating sepsis: Revealing the protective role of costunolide in a cecal ligation and puncture rat model.Iranian journal of basic medical sciences · 2024Article
- Nicotinamide mononucleotide as a therapeutic agent to alleviate multi-organ failure in sepsis.Journal of translational medicine · 2023Article
- Article
- Research progress on the activation mechanism of NLRP3 inflammasome in septic cardiomyopathy.Immunity, inflammation and disease · 2023Review
- Mitochondrial DNA Release in Innate Immune Signaling.Annual review of biochemistry · 2023Review
- Inflammatory mechanisms and intervention strategies for sepsis-induced myocardial dysfunction.Immunity, inflammation and disease · 2023Review
- The Role of Oxidative Stress Enhanced by Adiposity in Cardiometabolic Diseases.International journal of molecular sciences · 2023Review
- AMPK activation attenuates cancer-induced bone pain by reducing mitochondrial dysfunction-mediated neuroinflammation.Acta biochimica et biophysica Sinica · 2023Article
- Emerging roles of microRNAs in septic cardiomyopathy.Frontiers in pharmacology · 2023Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We have previously shown that mitochondria-targeted vitamin E (Mito-Vit-E), a mtROS specific antioxidant, improves cardiac performance and attenuates inflammation in a pneumonia-related sepsis model. In this study, we applied the same approaches to decipher the signaling pathway(s) of mtROS-dependent cardiac inflammation after sepsis. Sepsis was induced in Sprague Dawley rats by intratracheal injection of S. pneumoniae. Mito-Vit-E, vitamin E or vehicle was administered 30 minutes later. In myocardium 24 hours post-inoculation, Mito-Vit-E, but not vitamin E, significantly protected mtDNA integrity and decreased mtDNA damage. Mito-Vit-E alleviated sepsis-induced reduction in mitochondria-localized DNA repair enzymes including DNA polymerase γ, AP endonuclease, 8-oxoguanine glycosylase, and uracil-DNA glycosylase. Mito-Vit-E dramatically improved metabolism and membrane integrity in mitochondria, suppressed leakage of mtDNA into the cytoplasm, inhibited up-regulation of Toll-like receptor 9 (TLR9) pathway factors MYD88 and RAGE, and limited RAGE interaction with its ligand TFAM in septic hearts. Mito-Vit-E also deactivated NF-κB and caspase 1, reduced expression of the essential inflammasome component ASC, and decreased inflammatory cytokine IL-1β. In vitro, both Mito-Vit-E and TLR9 inhibitor OND-I suppressed LPS-induced up-regulation in MYD88, RAGE, ASC, active caspase 1, and IL-1β in cardiomyocytes. Since free mtDNA escaped from damaged mitochondria function as a type of DAMPs to stimulate inflammation through TLR9, these data together suggest that sepsis-induced cardiac inflammation is mediated, at least partially, through mtDNA-TLR9-RAGE. At last, Mito-Vit-E reduced the circulation of myocardial injury marker troponin-I, diminished apoptosis and amended morphology in septic hearts, suggesting that mitochondria-targeted antioxidants are a potential cardioprotective approach for sepsis.
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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.