ReviewFrontiers in immunology2025
Cell-free mitochondrial DNA as a pro-inflammatory agent in blood circulation: mechanisms, therapeutic implications, and clinical challenges in immune dysregulation.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed.
- Review
- Mitochondrial lipid remodeling in sepsis-associated acute kidney injury: a cardiolipin-centered convergence framework.Archives of toxicology · 2026Review
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Circulating Cell-Free DNA in Psychiatric Disorders: Current Evidence, Inflammation-Based Stratification, and Future Perspectives.International journal of molecular sciences · 2026Review
- Review
- ProbioticBrain sciences · 2026Article
- Circulating Clues in Ménière's Disease: Elevated Cell-Free DNA and a Pro-Inflammatory Signature in Patients' Blood.International journal of molecular sciences · 2026Article
- Beyond Decellularization: Remnant Mitochondrial DNA Can Act as Hidden Damage-Associated Molecular Pattern.Bioengineering (Basel, Switzerland) · 2026Article
- The role of exercise-mediated mitochondrial quality control remodeling in aging.Frontiers in cell and developmental biology · 2026Review
- Myocardial ischemia-reperfusion injury after acute myocardial infarction: spatiotemporal mechanisms and endotype-matched multi-target modulation by compounds from traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- Exosomal immune decoy integrates cfDNA scavenging and mTOR inhibition for synergistic lupus nephritis therapy.Theranostics · 2026Article
- Intercellular mitochondrial transfer in melanoma progression and therapeutic resistance: mechanisms and targeting potential.Frontiers in oncology · 2026Review
- NETosis-Related Biomarkers in Systemic Lupus Erythematosus, Rheumatoid Arthritis, Psoriatic Arthritis and Ankylosing Spondylitis: A Comparative Study.International journal of molecular sciences · 2025Article
- Mitochondrial DNA damage in HIV infection: a mechanistic driver of immunometabolic dysfunction and chronic inflammation.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circulating cf-mtDNA has emerged as a dual-functional entity in human pathophysiology, serving not only as a disease biomarker but also as a potent innate immune activator through its molecular pattern recognition. Extracellular mtDNA engages PRRs, triggering dysregulated pro-inflammatory signaling in multiple cell lineages. Elevated mtDNA in circulation correlates with pathogenesis of autoimmune disorders, infectious diseases, critical illnesses, neurological disorders, and hematological abnormalities. Therapeutic strategies combining mtDNA monitoring with inhibitors targeting its release mechanisms and downstream pathways offer novel immunomodulatory strategies. This review systematically examines the therapeutic nexus of blood-derived mtDNA in immune activation and disease progression. Here we aim to elucidate the function of mtDNA in disease pathobiology while highlighting mitochondria's central position in human systemic homeostasis.
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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 Socratic graph.