ArticleFrontiers in cell and developmental biology2020
Mitophagy-Mediated mtDNA Release Aggravates Stretching-Induced Inflammation and Lung Epithelial Cell Injury via the TLR9/MyD88/NF-κB Pathway.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Mitophagy in cisplatin-induced kidney injury: regulatory mechanisms and therapeutic targets.Annals of medicine · 2026Review
- Maternal hyperhomocysteinemia promotes adverse pregnancy outcomes via mtDNA-cGAS-STING signaling-mediated trophoblast mitophagy.Redox biology · 2026Article
- AQP4-IgG-Induced Astrocyte-Derived Small Extracellular Vesicles Carrying Mitochondrial DNA Regulate the TLR9/MyD88/NF-κB Pathway to Drive Microglial Activation and Neuromyelitis Optica.Neurochemical research · 2026Article
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial-targeted actions of lycopene: evidence, mechanisms and future directions.Frontiers in pharmacology · 2026Review
- TLR9/MyD88/NF-κB signaling mediates mental stress-induced exacerbation of psoriasis through immune dysregulation in a mouse model.PloS one · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- The hidden driver of osteoporosis: mitochondria-dominated inflammation.Cell communication and signaling : CCS · 2025Review
- Double-edged mitophagy: balancing inflammation and resolution in lung disease.Clinical science (London, England : 1979) · 2025Review
- Cell-Free Circulating Mitochondrial DNA Levels Following High-Frequency Jet Ventilation-A Post Hoc Analysis.Journal of clinical medicine · 2025Article
- DAMPs cross-talk interpretation of MDD mechanisms.Science advances · 2025Review
- Recent advances and applications of mitochondria in tumors and inflammation.Journal of translational medicine · 2025Review
- CDDO-imidazolide ameliorates sepsis-induced ARDS by enhancing mitophagy via the Nrf2 pathway to prohibit alveolar macrophage pyroptosis and HMGB1 release.Acta biochimica et biophysica Sinica · 2025Article
- Mitophagy in relation to chronic inflammation/ROS in aging.Molecular and cellular biochemistry · 2025Review
- Cyclophilin D (PPIF) and MPTP in hepatic ischemia-reperfusion injury: insights into mechanisms.Frontiers in immunology · 2025Review
- Gut microbiota-mitochondrial crosstalk in obesity: novel mechanistic insights and therapeutic strategies with traditional Chinese medicine.Frontiers in pharmacology · 2025Review
- Ferritinophagy mediated by the AMPK/ULK1 pathway is involved in ferroptosis subsequent to ventilator-induced lung injury.Respiratory research · 2024Article
- Capsaicin mitigates ventilator-induced lung injury by suppressing ferroptosis and maintaining mitochondrial redox homeostasis through SIRT3-dependent mechanisms.Molecular medicine (Cambridge, Mass.) · 2024Article
- Molecular mechanism and potential role of mitophagy in acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- mtDNA release promotes cGAS-STING activation and accelerated aging of postmitotic muscle cells.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn animal models of ventilation-induced lung injury, mitophagy triggers mitochondria damage and the release of mitochondrial (mt) DNA, which activates inflammation. However, the mechanism of this process is unclear.
methodsA model of cyclic stretching (CS)-induced lung epithelial cell injury was established. The genetic intervention of phosphatase and tensin homolog-induced kinase 1 (PINK1) expression via lentivirus transfection was used to identify the relationship between PINK1-mediated mitophagy and mtDNA release in stretching-induced inflammatory response and injury. Pharmacological inhabitation of Toll-like receptor 9 (TLR9) and myeloid differentiation factor 88 (MyD88) expression was performed via their related inhibitors, while pre-treatment of exogenous mtDNA was used to verify the role of mtDNA in stretching-induced inflammatory response and injury.
resultsUsing a cell culture model of CS, we found that knocking down PINK1 in lung epithelial cells reduced mitophagy activation and mtDNA release, leading to milder inflammatory response and injury; conversely, up-regulating PINK1 exacerbated stretching-induced inflammation and injury, and similar effects were observed by upregulating TLR9 to induce expression of MyD88 and nuclear factor-κB (NF-κB)/p65. Down-regulating MyD88 protected lung epithelial cells from stretching injury and decreased NF-κB/p65 expression.
conclusionThese findings suggest that PINK1-dependent mitophagy and associated TLR9 activation is indeed a major factor in stretch-induced cell injury via a mechanism in which released mtDNA activates TLR9 and thereby the MyD88/NF-κB pathway. Inhibiting this process may be a therapeutic approach to prevent inflammation and cell injury in patients on mechanical ventilation.
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