ArticlePloS one2013
Mitochondrial DAMPs increase endothelial permeability through neutrophil dependent and independent pathways.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 212 citations in OpenAlex.
- Elevated levels of plasma mitochondrial DNA DAMPs are linked to clinical outcome in severely injured human subjects.Annals of surgery · 2013Trial
- Reduced ALDH2 Activity and Cardiovascular Carbonyl Stress: From Reactive Aldehyde Networks to Coronary Microvascular Obstruction.Cardiovascular toxicology · 2026Review
- Formyl peptide receptor 1 agonism selectively suppresses mitochondria-driven neutrophil extracellular trap formation while preserving antibacterial immunity.Molecular medicine (Cambridge, Mass.) · 2026Article
- Damage-Associated Molecular Patterns in Perioperative Anesthesia Care: A Clinical Perspective.Anesthesia research · 2026Article
- Revisiting osteoarthritis pathogenesis through the lens of cGAS-STING: Mitochondrial damage, pyroptosis, and inflammatory cascades.Journal of orthopaedic translation · 2026Review
- Mitochondrial DNA efflux as a potential amplifier of systemic inflammatory network rewiring in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Kidney mitochondrial DNA contributes to systemic IL-6 release in sepsis-associated acute kidney injury.JCI insight · 2025Article
- Unlocking the potential of uncontrolled DCD in lung transplantation: A review of 2 decades of experience.JHLT open · 2025Review
- Unlocking the potential of mitochondrial transplantation: overcoming challenges and paving the way for routine therapeutic application.Cytotechnology · 2025Review
- Pulmozyme Ameliorates LPS-Induced Lung Fibrosis but Provokes Residual Inflammation by Modulating Cell-Free DNA Composition and Controlling Neutrophil Phenotype.Biomolecules · 2025Article
- Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Acute lung injury and post-cardiac arrest syndrome: a narrative review.Journal of intensive care · 2024Review
- Early identification and diagnosis, pathophysiology, and treatment of sepsis-related acute lung injury: a narrative review.Journal of thoracic disease · 2024Review
- Mitochondrial function in lungs of rats with different susceptibilities to hyperoxia-induced acute lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Endothelial cell dynamics in sepsis-induced acute lung injury and acute respiratory distress syndrome: pathogenesis and therapeutic implications.Cell communication and signaling : CCS · 2024Review
- Bovine lactoferrin inhibits inflammatory response and apoptosis in lipopolysaccharide-induced acute lung injury by targeting the PPAR-γ pathway.Molecular biology reports · 2024Article
- Mast Cells in Autism Spectrum Disorder-The Enigma to Be Solved?International journal of molecular sciences · 2024Review
- Extracellular vesicles in acute respiratory distress syndrome: Understanding protective and harmful signaling for the development of new therapeutics.Histology and histopathology · 2024Review
- Trained innate immunity as a potential link between preeclampsia and future cardiovascular disease.Frontiers in endocrinology · 2024Review
- Hepatic Macrophages as Targets for the MSC-Based Cell Therapy in Non-Alcoholic Steatohepatitis.Biomedicines · 2023Review
57 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Trauma and sepsis can cause acute lung injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) in part by triggering neutrophil (PMN)-mediated increases in endothelial cell (EC) permeability. We had shown that mitochondrial (mt) damage-associated molecular patterns (DAMPs) appear in the blood after injury or shock and activate human PMN. So we now hypothesized that mitochondrial DAMPs (MTD) like mitochondrial DNA (mtDNA) and peptides might play a role in increased EC permeability during systemic inflammation and proceeded to evaluate the underlying mechanisms. MtDNA induced changes in EC permeability occurred in two phases: a brief, PMN-independent 'spike' in permeability was followed by a prolonged PMN-dependent increase in permeability. Fragmented mitochondria (MTD) caused PMN-independent increase in EC permeability that were abolished with protease treatment. Exposure to mtDNA caused PMN-EC adherence by activating expression of adherence molecule expression in both cell types. Cellular activation was manifested as an increase in PMN calcium flux and EC MAPK phosphorylation. Permeability and PMN adherence were attenuated by endosomal TLR inhibitors. EC lacked formyl peptide receptors but were nonetheless activated by mt-proteins, showing that non-formylated mt-protein DAMPs can activate EC. Mitochondrial DAMPs can be released into the circulation by many processes that cause cell injury and lead to pathologic endothelial permeability. We show here that mitochondria contain multiple DAMP motifs that can act on EC and/or PMN via multiple pathways. This can enhance PMN adherence to EC, activate PMN-EC interactions and subsequently increase systemic endothelial permeability. Mitochondrial DAMPs may be important therapeutic targets in conditions where inflammation pathologically increases endothelial permeability.
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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 OpenQuestion graph.