Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases
Open accessAbstract
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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The interaction of dECM scaffolds with the innate immune system is mainly mediated via DAMPs, danger signals released upon cell and ECM damage during graft processing or implantation.
“The interaction of dECM scaffolds with the innate immune system is mainly mediated via damage-associated molecular patterns (DAMPs), danger signals released upon the cell and ECM damage during graft processing or implantation.”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [36]
The Introduction says mitochondrial DAMPs are released after cellular stress or death and stimulate the innate immune system. The paper does not address dECM scaffolds, ECM damage during graft processing or implantation, or whether DAMPs are the main mediator of scaffold–immune interactions. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNuclear and mitochondrial DNA, ROS, and fragmented ECM components such as hyaluronic acid or fibronectin are among the most renowned DAMPs.
“Nuclear and mitochondrial DNA, reactive oxygen species (ROS), and fragmented ECM components such as hyaluronic acid or fibronectin are among the most renowned DAMPs, which are released due to perturbation in the arrangement of nucleic acids within cells, transplantation imperfections such as ischemia-reperfusion, and harsh decellularization strategies, respectively [34–37].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [36]
The Introduction identifies mitochondrial DNA as an important DAMP. The passages on mtDNA and inflammation describe ROS as a source of oxidative damage to mtDNA, not as a DAMP itself; they do not identify nuclear DNA, hyaluronic acid, or fibronectin as DAMPs. Thus this source supports only the mitochondrial-DNA item in the attributed list. (LLM, conf=0.88)
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- Authors
- Nakayama, H., & Otsu, K.
- Affiliations
- The University of Osaka (JP)
- King's College London (GB)
- Corresponding author
- Otsu, Kinya
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2018-03-06
- Volume
- 475
- Issue
- 5
- Pages
- 839-852
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC5840331
- OpenAlex
- W2791281024
- Cited by
- 160
- References
- 121
- Citations by year
- 2026: 21 · 2025: 13 · 2024: 21 · 2023: 19 · 2022: 25 · 2021: 19 · 2020: 23 · 2019: 19
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Biochemical Journal (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (CH/11/3/29051, RG/16/15/32294)
- Ministry of Education, Culture, Sports, Science and Technology
- Japan Society for the Promotion of Science (17K09576)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- mitochondrial DNA, sterile inflammation, cardiac inflammation, heart failure, damage-associated molecular patterns, pattern recognition receptors, TLR9, NOD-like receptors, cGAS, interferon-stimulated genes, nuclear factor-kappaB, interferon regulatory factors, inflammatory cytokines, mitochondrial reactive oxygen species, cardiovascular disease
- MeSH terms
- Animals, Cardiovascular Diseases, DNA, Mitochondrial, Humans, Inflammation, Inflammation Mediators
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