ArticleAmerican journal of respiratory and critical care medicine2017
Extracellular Mitochondrial DNA Is Generated by Fibroblasts and Predicts Death in Idiopathic Pulmonary Fibrosis.
Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.
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Who cites it
118 citing papers in PubMed, 170 citations in OpenAlex.
- Advances in metabolic reprogramming of pulmonary fibrosis.Chinese medical journal pulmonary and critical care medicine · 2026Review
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- Mitochondria Meet the Lung Microbiome: A Bidirectional Dialogue in Inflammation and Respiratory Diseases.Biomedicines · 2026Review
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- High density lipoproteins, disease severity and clinical outcomes in patients with idiopathic pulmonary fibrosis.Respiratory research · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Precision Medicine Advances in Chronic Lung Diseases.International journal of molecular sciences · 2025Article
- Cyclic GMP-AMP synthase expression is enhanced in systemic sclerosis-associated interstitial lung disease and stimulates inflammatory myofibroblast activation.The European respiratory journal · 2025Article
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Damage sensing through TLR9 regulates inflammatory and antiviral responses during influenza infection.Mucosal immunology · 2025Article
- Coexisting Lung Cancer and Pulmonary Tuberculosis: A Comprehensive Review From Incidence to Management.Cancer reports (Hoboken, N.J.) · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Review
- Deciphering the interplay: circulating cell-free DNA, signaling pathways, and disease progression in idiopathic pulmonary fibrosis.3 Biotech · 2025Review
- MitochondrialInternational journal of molecular sciences · 2025Article
- Deciphering the Correlation between the Emergence of Lung Carcinoma Associated with Tuberculosis-related Inflammation.Endocrine, metabolic & immune disorders drug targets · 2025Review
- Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2025Article
- Cigarette Smoke Extract-Induced Necroptosis Causes Mitochondrial DNA Release and Inflammation of Bronchial Epithelial Cells.International journal of chronic obstructive pulmonary disease · 2025Article
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
58 more citing papers are in PubMed but not listed here.
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Authors and funding
28 authors at 6 institutions in 2 countries.
Funding
Abstract
rationaleIdiopathic pulmonary fibrosis (IPF) involves the accumulation of α-smooth muscle actin-expressing myofibroblasts arising from interactions with soluble mediators such as transforming growth factor-β1 (TGF-β1) and mechanical influences such as local tissue stiffness. Whereas IPF fibroblasts are enriched for aerobic glycolysis and innate immune receptor activation, innate immune ligands related to mitochondrial injury, such as extracellular mitochondrial DNA (mtDNA), have not been identified in IPF.
objectivesWe aimed to define an association between mtDNA and fibroblast responses in IPF.
methodsWe evaluated the response of normal human lung fibroblasts (NHLFs) to stimulation with mtDNA and determined whether the glycolytic reprogramming that occurs in response to TGF-β1 stimulation and direct contact with stiff substrates, and spontaneously in IPF fibroblasts, is associated with excessive levels of mtDNA. We measured mtDNA concentrations in bronchoalveolar lavage (BAL) from subjects with and without IPF, as well as in plasma samples from two longitudinal IPF cohorts and demographically matched control subjects. MEASUREMENTS AND MAIN
resultsExposure to mtDNA augments α-smooth muscle actin expression in NHLFs. The metabolic changes in NHLFs that are induced by interactions with TGF-β1 or stiff hydrogels are accompanied by the accumulation of extracellular mtDNA. These findings replicate the spontaneous phenotype of IPF fibroblasts. mtDNA concentrations are increased in IPF BAL and plasma, and in the latter compartment, they display robust associations with disease progression and reduced event-free survival.
conclusionsThese findings demonstrate a previously unrecognized and highly novel connection between metabolic reprogramming, mtDNA, fibroblast activation, and clinical outcomes that provides new insight into IPF.
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