ArticleIntensive care medicine2012
Src tyrosine kinase inhibition prevents pulmonary ischemia-reperfusion-induced acute lung injury.
Article in Intensive care medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Non-receptor tyrosine kinase signaling pathways and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Pterostilbene attenuates lung ischemia-reperfusion injury: integrative insights from network pharmacology, molecular dynamics, and experimental validation.Frontiers in pharmacology · 2026Article
- Proteome-wide mendelian randomization identifies causal plasma proteins in interstitial lung disease.Scientific reports · 2025Article
- Quercetin as a therapeutic agent activate the Nrf2/Keap1 pathway to alleviate lung ischemia-reperfusion injury.Scientific reports · 2024Article
- Cellular and molecular mechanisms of cell damage and cell death in ischemia-reperfusion injury in organ transplantation.Molecular biology reports · 2024Review
- Oxidative stress in acute pulmonary embolism: emerging roles and therapeutic implications.Thrombosis journal · 2024Review
- Unphysiological lung strain promotes ventilation-induced lung injury via activation of the PECAM-1/Src/STAT3 signaling pathway.Frontiers in pharmacology · 2024Article
- Review
- Screening gene signatures for clinical response subtypes of lung transplantation.Molecular genetics and genomics : MGG · 2022Article
- Ruscogenin alleviates LPS-triggered pulmonary endothelial barrier dysfunction through targeting NMMHC IIA to modulate TLR4 signaling.Acta pharmaceutica Sinica. B · 2022Article
- The dynamic changes in autophagy activity and its role in lung injury after deep hypothermic circulatory arrest.Journal of cellular and molecular medicine · 2022Article
- Salvianolic Acid A Protects against Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting Neutrophil NETosis.Oxidative medicine and cellular longevity · 2022Article
- Multi-omics data integration and network-based analysis drives a multiplex drug repurposing approach to a shortlist of candidate drugs against COVID-19.Briefings in bioinformatics · 2021Article
- Bletinib ameliorates neutrophilic inflammation and lung injury by inhibiting Src family kinase phosphorylation and activity.British journal of pharmacology · 2021Article
- Targeting Ferroptosis for Lung Diseases: Exploring Novel Strategies in Ferroptosis-Associated Mechanisms.Oxidative medicine and cellular longevity · 2021Review
- Bioinformatic identification of hub genes and key pathways in neutrophils of patients with acute respiratory distress syndrome.Medicine · 2020Article
- Highlighted STAT3 as a potential drug target for cancer therapy.BMB reports · 2019Review
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- Ventilator-induced diaphragm dysfunction in critical illness.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Intracellular signal transduction pathways as potential drug targets for ischemia-reperfusion injury in lung transplantation.Journal of thoracic disease · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
purposePulmonary ischemia-reperfusion is a pathological process seen in several clinical conditions, including lung transplantation, cardiopulmonary bypass, resuscitation for circulatory arrest, atherosclerosis, and pulmonary embolism. A better understanding of its molecular mechanisms is very important.
methodsRat left lung underwent in situ ischemia for 60 min, followed by 2 h of reperfusion. The gene expression profiles and Src protein tyrosine kinase (PTK) phosphorylation were studied over time, and PP2, an Src PTK inhibitor, was intravenously administered 10 min before lung ischemia to determine the role of Src PTK in lung injury.
resultsReperfusion following ischemia significantly changed the expression of 169 genes, with Mmp8, Mmp9, S100a9, and S100a8 being the most upregulated genes. Ischemia alone only affected expression of 9 genes in the lung. However, Src PTK phosphorylation (activation) was increased in the ischemic lung, mainly on the alveolar wall. Src PTK inhibitor pretreatment decreased phosphorylation of Src PTKs, total protein tyrosine phosphorylation, and STAT3 phosphorylation. It increased phosphorylation of the p85α subunit of PI3 kinase, a signal pathway that can inhibit coagulation and inflammation. PP2 reduced leukocyte infiltration in the lung, apoptotic cell death, fibrin deposition, and severity of acute lung injury after reperfusion. Src inhibition also significantly reduced CXCL1 (GRO/KI) and CCL2 (MCP-1) chemokine levels in the serum.
conclusionDuring pulmonary ischemia, Src PTK activation, rather than alteration in gene expression, may play a critical role in reperfusion-induced lung injury. Src PTK inhibition presents a new prophylactic treatment for pulmonary ischemia-reperfusion-induced acute lung injury.
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