ReviewAmerican journal of physiology. Lung cellular and molecular physiology2014
Shear stress-related mechanosignaling with lung ischemia: lessons from basic research can inform lung transplantation.
Review in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 112 citations in OpenAlex.
- Key role of the endothelium in lung ischemia-reperfusion injury: What the clinician needs to know.JHLT open · 2026Review
- Passive versus active right ventricular support during lung transplantation: Insights from a porcine pulmonary ischemia-reperfusion injury model.JTCVS techniques · 2026Article
- The Role of the Endothelium as a Key Regulator of Chronic Transplant Rejection.Results and problems in cell differentiation · 2026Review
- Epigenetic regulation in transplant rejection and tolerance: mechanisms and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
- Lung Ischemia-Reperfusion Injury in Lung Transplant Surgery: Where Do We Stand?Antioxidants (Basel, Switzerland) · 2025Review
- Impact of Venous CONgestion on Organ Function and Outcomes in Sepsis (ICON-Sepsis): a prospective observational cohort study protocol.BMJ open · 2025Article
- Mechanical stress facilitates calcium influx and growth of alveolar epithelial cells via activation of the BDKRB1/CaRespiratory research · 2025Article
- Endothelial ENaC-α Restrains Oxidative Stress in Lung Capillaries in Murine Pneumococcal Pneumonia-associated Acute Lung Injury.American journal of respiratory cell and molecular biology · 2025Article
- Primary graft dysfunction after Lung transplantation: unveiling the role of innate immunity.Clinical and experimental immunology · 2025Article
- Machine learning-based prediction model for lung ischemia-reperfusion injury: insights from disulfidptosis-related genes.Frontiers in pharmacology · 2025Article
- Experimental Lung Transplantation Related With HIF-1, VEGF, ROS. Assessment of HIF-1alpha, VEGF, and Reactive Oxygen Species After Competitive Blockade of Chetomin for Lung Transplantation in Rats.Physiological research · 2024Article
- Low Calcium-High Magnesium Krebs-Henseleit Solution Combined with Adenosine and Lidocaine Improved Rat Aortic Function and Structure Following Cold Preservation.Medicina (Kaunas, Lithuania) · 2024Article
- Energy Metabolism and Metformin: Effects on Ischemia-Reperfusion Injury in Kidney Transplantation.Biomedicines · 2024Review
- The endothelium: gatekeeper to lung ischemia-reperfusion injury.Respiratory research · 2024Review
- Advances in lung ischemia/reperfusion injury: unraveling the role of innate immunity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- Ex Vivo Optimization of Donor Lungs with Inhaled Sevoflurane during Normothermic Ex Vivo Lung Perfusion (VITALISE): A Pilot and Feasibility Study in Sheep.International journal of molecular sciences · 2024Article
- Oxidative stress in acute pulmonary embolism: emerging roles and therapeutic implications.Thrombosis journal · 2024Review
- Reactive oxygen species in endothelial signaling in COVID-19: Protective role of the novel peptide PIP-2.PloS one · 2024Article
- The hemodynamic interplay between pulmonary ischemia-reperfusion injury and right ventricular function in lung transplantation: a translational porcine model.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Acellular ex vivo lung perfusate silences pro-inflammatory signaling in human lung endothelial and epithelial cells.Journal of translational medicine · 2023Article
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Abstract
Cessation of blood flow represents a physical event that is sensed by the pulmonary endothelium leading to a signaling cascade that has been termed "mechanotransduction." This paradigm has clinical relevance for conditions such as pulmonary embolism, lung bypass surgery, and organ procurement and storage during lung transplantation. On the basis of our findings with stop of flow, we postulate that normal blood flow is "sensed" by the endothelium by virtue of its location at the interface of the blood and vessel wall and that this signal is necessary to maintain the endothelial cell membrane potential. Stop of flow is sensed by a "mechanosome" consisting of PECAM-VEGF receptor-VE cadherin that is located in the endothelial cell caveolae. Activation of the mechanosome results in endothelial cell membrane depolarization that in turn leads to activation of NADPH oxidase (NOX2) to generate reactive oxygen species (ROS). Endothelial depolarization additionally results in opening of T-type voltage-gated Ca(2+) channels, increased intracellular Ca(2+), and activation of nitric oxide (NO) synthase with resultant generation of NO. Increased NO causes vasodilatation whereas ROS provide a signal for neovascularization; however, with lung transplantation overproduction of ROS and NO can cause oxidative injury and/or activation of proteins that drive inflammation and cell death. Understanding the key events in the mechanosignaling cascade has important lessons for the design of strategies or interventions that may reduce injury during storage of donor lungs with the goal to increase the availability of lungs suitable for donation and thus improving access to lung transplantation.
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