ReviewFrontiers in immunology2022
Role of released mitochondrial DNA in acute lung injury.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- cGAS-STING pathway activation drives the cold-to-hot tumor transition and sensitizes immunotherapy.Cancer biology & medicine · 2026Review
- Mitochondrial transplantation in lung diseases: From mechanisms to application prospects.Genes & diseases · 2026Review
- Review
- L-Arginine-Modified Chitosan Curcumin Nanocrystals Target M1 Macrophages via CAT-2/Clathrin-Mediated Endocytosis for Mitochondrial Protection and ALI/ARDS Therapy.Pharmaceutics · 2026Article
- Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation.Toxics · 2026Review
- Mitochondrial-related biomarkers as the diagnostic markers in sepsis induced acute respiratory distress syndrome.European journal of medical research · 2026Article
- Endothelial-Epithelial Crosstalk Drives Alveolar-Capillary Barrier Dysfunction in ARDS.Journal of inflammation research · 2026Review
- Cell-specific exosomes in sepsis-associated ARDS: from immunometabolic reprogramming to precision medicine.Frontiers in immunology · 2026Review
- Novel Carbon Dots Nanomaterials for the Precision Diagnosis and Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome: Mechanisms and Applications.International journal of nanomedicine · 2026Review
- The cGAS-STING pathway in pulmonary infectious and sterile inflammation: differences, connections, and therapeutic implications.Frontiers in immunology · 2026Review
- Mitochondrial 8-Oxoguanine DNA Glycosylase 1-Mitochondrial Permeability Transition Pore Axis Drives Mitochondrial DNA Escape and Accelerates Osteoarthritis Progression.Research (Washington, D.C.) · 2026Article
- Onion-Mitochondria Inhibit Lipopolysaccharide-Induced Acute Lung Injury by Shaping Lung Macrophage Mitochondrial Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial DNA haplogroups and circulating cell-free mitochondrial DNA as biomarkers of bronchopulmonary dysplasia.Pediatric research · 2025Article
- MSC-mediated mitochondrial transfer promotes metabolic reprograming in endothelial cells and vascular regeneration in ARDS.Redox report : communications in free radical research · 2025Article
- Mitochondrial transplantation attenuates alveolar epithelial cell dysfunction and reduces disruption of tight junction proteins to alleviate lung ischaemia-reperfusion injury.Journal of translational medicine · 2025Article
- Article
- The cGAS-STING Pathway in Pulmonary Diseases: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Cell-Free Circulating Mitochondrial DNA Levels Following High-Frequency Jet Ventilation-A Post Hoc Analysis.Journal of clinical medicine · 2025Article
- Inhibition of STING-induced mitochondrial Drp1/N-GSDMD-mediated MtDNA release alleviates Sepsis-induced lung injury.Cellular and molecular life sciences : CMLS · 2025Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS) is a form of acute-onset hypoxemic respiratory failure characterised by an acute, diffuse, inflammatory lung injury, and increased alveolar-capillary permeability, which is caused by a variety of pulmonary or nonpulmonary insults. Recently, aberrant mitochondria and mitochondrial DNA(mtDNA) level are associated with the development of ALI/ARDS, and plasma mtDNA level shows the potential to be a promising biomarker for clinical diagnosis and evaluation of lung injury severity. In mechanism, the mtDNA and its oxidised form, which are released from impaired mitochondria, play a crucial role in the inflammatory response and histopathological changes in the lung. In this review, we discuss mitochondrial outer membrane permeabilisation (MOMP), mitochondrial permeability transition pore(mPTP), extracellular vesicles (EVs), extracellular traps (ETs), and passive release as the principal mechanisms for the release of mitochondrial DNA into the cytoplasm and extracellular compartments respectively. Further, we explain how the released mtDNA and its oxidised form can induce inflammatory cytokine production and aggravate lung injury through the Toll-like receptor 9(TLR9) signalling, cytosolic cGAS-stimulator of interferon genes (STING) signalling (cGAS-STING) pathway, and inflammasomes activation. Additionally, we propose targeting mtDNA-mediated inflammatory pathways as a novel therapeutic approach for treating ALI/ARDS.
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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.