ReviewThe Biochemical journal2018
Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases.
Review in The Biochemical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
103 citing papers in PubMed, 154 citations in OpenAlex.
- Boosting NAD level suppresses inflammatory activation of PBMCs in heart failure.The Journal of clinical investigation · 2020Trial
- Admission serum mitochondrial DNA relative abundance is associated with angiographic no-reflow or slow-flow after primary percutaneous coronary intervention in STEMI.Journal of thrombosis and thrombolysis · 2026Article
- MA-5 attenuates disease-associated transcriptomic aging and pathological microglial states in Gaucher disease.Research square · 2026Article
- Review
- Carnosinylation of Cardiac Antigens Attenuates Immunogenic Responses and Improves Function in Failing Hearts.Journal of the American Heart Association · 2026Article
- Association of mitochondrial DNA haplogroup, oxidative DNA damage and inflammatory markers in middle-aged adults.International journal of radiation biology · 2026Article
- Endothelial Mitochondrial Dysfunction in INOCA and Coronary Microvascular Dysfunction: Mechanisms, Sex Differences, and Therapeutic Implications.Journal of cardiovascular development and disease · 2026Review
- Factors Modulating Mitochondrial Function after Arterial Injury: Past-to-Present Evidence for the Devising of Future Preventive and Therapeutic Strategies.Journal of cardiovascular translational research · 2026Review
- Dynamic regulation of the 'mitochondria‑immune axis' in myocardial infarction: Molecular mechanisms driving macrophage polarization through energy metabolism disorders (Review).Molecular medicine reports · 2026Review
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Preliminary exploration of dynamic changes in circulating mitochondrial DNA (ΔmtDNA) as a prognostic biomarker for acute ST-segment elevation myocardial infarction patients: a prospective observational study.BMC cardiovascular disorders · 2026Observational
- Circulating Mitochondrial DNA Aggravates Post-Ischemic Functional and Metabolic Recovery in an Isolated Rat Heart Model of Donation After Circulatory Death.International journal of molecular sciences · 2026Article
- Mitochondrial dysfunction in endothelial senescence: implications for vascular remodeling and therapeutic strategies.Archives of pharmacal research · 2026Review
- Finerenone after FINEARTS-HF: evidence boundaries and implementation in heart failure with LVEF ≥40.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial transfer as a driver of immune microenvironment remodeling.Frontiers in immunology · 2026Review
- Understanding cardiovascular aging as a disorder of mitochondrial network.The journal of cardiovascular aging · 2026Article
- Emerging microbiome-mitochondria crosstalk in host defense and infectious diseases: mechanistic insights into NLRP3 inflammasome activation and mtDNA-mediated immunomodulation.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- Oxidative Stress, Mitochondrial Quality Control, Autophagy, and Sirtuins in Heart Failure.International journal of molecular sciences · 2025Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection - termed sterile inflammation - is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs). Mitochondria release multiple DAMPs including mitochondrial DNA, peptides, and lipids, which induce inflammation via the stimulation of multiple PRRs. Among the mitochondrial DAMPs, mitochondrial DNA (mtDNA) is currently highlighted as the DAMP that mediates the activation of multiple PRRs, including Toll-like receptor 9, Nod-like receptors, and cyclic GMP-AMP synthetase/stimulator of interferon gene pathways. These PRR signalling pathways, in turn, lead to the activation of nuclear factor-κB and interferon regulatory factor, which enhances the transcriptional activity of inflammatory cytokines and interferons, and induces the recruitment of inflammatory cells. As the heart is an organ comprising abundant mitochondria for its ATP consumption (needed to maintain constant cyclic contraction and relaxation), the generation of massive amounts of mitochondrial radical oxygen species and mitochondrial DAMPs are predicted to occur and promote cardiac inflammation. Here, we will focus on the role of mtDNA in cardiac inflammation and review the mechanism and pathological significance of mtDNA-induced inflammatory responses in cardiac diseases.
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What OpenQuestion holds
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.