ArticleThe Journal of clinical investigation2003
Mechano-oxidative coupling by mitochondria induces proinflammatory responses in lung venular capillaries.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- A Barrier to Defend - Models of Pulmonary Barrier to Study Acute Inflammatory Diseases.Frontiers in immunology · 2022Pooled it
- Inhaled General Anesthetics in Alzheimer's Disease Progression: Divergent Effects, Underlying Mechanisms, and Future Perspectives.Molecular neurobiology · 2026Review
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Bioenergetics and metabolism of the pulmonary endothelium. Scientific session I: ReSPIRE 2025.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- The Reciprocal Relationship Between Cell Adhesion Molecules and Reactive Oxygen Species.Cells · 2025Review
- Epigallocatechin Gallate inPharmaceuticals (Basel, Switzerland) · 2025Article
- Bioactive Nanomaterials: Comprehensive Monitoring and Regulation of Acute Pancreatitis Induced Acute Lung Injury.International journal of nanomedicine · 2025Review
- Senescence Rejuvenation through Reduction in Mitochondrial Reactive Oxygen Species Generation byAntioxidants (Basel, Switzerland) · 2024Article
- Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Nrf-2/ROS/NF-κB pathway is modulated by cynarin in human mesenchymal stem cells in vitro from ankylosing spondylitis.Clinical and translational science · 2024Article
- Engineered Dual Antioxidant Enzyme Complexes Targeting ICAM-1 on Brain Endothelium Reduce Brain Injury-Associated Neuroinflammation.Bioengineering (Basel, Switzerland) · 2024Article
- Mitochondria of lung venular capillaries mediate lung-liver cross talk in pneumonia.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Does Decreased Diffusing Capacity of the Lungs for Carbon Monoxide Constitute a Risk of Decompression Sickness in Occupational Divers?International journal of environmental research and public health · 2023Observational
- Immunomodulatory Properties of Natural Extracts and Compounds Derived fromPharmaceutics · 2023Review
- The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.International journal of molecular sciences · 2023Review
- Regulatory Components of Oxidative Stress and Inflammation and Their Complex Interplay in Carcinogenesis.Applied biochemistry and biotechnology · 2023Review
- Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- The mitochondrial calcium uniporter of pulmonary type 2 cells determines severity of acute lung injury.Nature communications · 2022Article
- Calcium-Permeable Channels and Endothelial Dysfunction in Acute Lung Injury.Current issues in molecular biology · 2022Review
- Delineation of Neuroprotective Effects and Possible Benefits of AntioxidantsTherapy for the Treatment of Alzheimer's Diseases by Targeting Mitochondrial-Derived Reactive Oxygen Species: Bench to Bedside.Molecular neurobiology · 2022Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Elevation of lung capillary pressure causes exocytosis of the leukocyte adhesion receptor P-selectin in endothelial cells (ECs), indicating that lung ECs generate a proinflammatory response to pressure-induced stress. To define underlying mechanisms, we followed the EC signaling sequence leading to P-selectin exocytosis through application of real-time, in situ fluorescence microscopy in lung capillaries. Pressure elevation increased the amplitude of cytosolic Ca(2+) oscillations that triggered increases in the amplitude of mitochondrial Ca(2+) oscillations and in reactive oxygen species (ROS) production. Responses to blockers of the Ca(2+) oscillations and of mitochondrial electron transport indicated that the ROS production was Ca(2+) dependent and of mitochondrial origin. A new proinflammatory mechanism was revealed in that pressure-induced exocytosis of P-selectin was inhibited by both antioxidants and mitochondrial inhibitors, indicating that the exocytosis was driven by mitochondrial ROS. In this signaling pathway mitochondria coupled pressure-induced Ca(2+) oscillations to the production of ROS that in turn acted as diffusible messengers to activate P-selectin exocytosis. These findings implicate mitochondrial mechanisms in the lung's proinflammatory response to pressure elevation and identify mitochondrial ROS as critical to P-selectin exocytosis in lung capillary ECs.
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What OpenQuestion holds
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.