ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Autophagy inhibitor 3-methyladenine protects against endothelial cell barrier dysfunction in acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 74 citations in OpenAlex.
- Article
- Autophagy in Acute Lung Injury.Cell biochemistry and biophysics · 2025Review
- mTOR and autophagy in acute lung injury pathogenesis and therapeutic potential.Journal of thoracic disease · 2025Review
- Serum metabolomics analysis reveals a novel association between maternal metabolism and fetal survival in sows fed diets containing differing methionine levels and sources.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Ferritinophagy mediated by the AMPK/ULK1 pathway is involved in ferroptosis subsequent to ventilator-induced lung injury.Respiratory research · 2024Article
- [3-Methyladenine alleviates early renal injury in diabetic mice by inhibiting AKT signaling].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Effect of Nano-selenium on Biological Mechanism of Goblet Cells of the Small Intestine Within Laying Hen.Biological trace element research · 2024Article
- Vitamin D3 improved hypoxia-induced lung injury by inhibiting the complement and coagulation cascade and autophagy pathway.BMC pulmonary medicine · 2024Article
- Spinal cord injury enhances lung inflammation and exacerbates immune response following exposure to LPS.Frontiers in immunology · 2024Article
- Based on Bioinformatics to Explore the Mechanism of "Tangzhiqing" Decoction Alleviating Type 2 Diabetes-associated Cognitive Dysfunction in Mice by Regulating Hippocampal Neuron Apoptosis and Autophagy.Combinatorial chemistry & high throughput screening · 2024Article
- Capsaicin Attenuates LPS-Induced Acute Lung Injury by Inhibiting Inflammation and Autophagy Through Regulation of the TRPV1/AKT Pathway.Journal of inflammation research · 2024Article
- Spleen Tyrosine Kinase phosphorylates VE-cadherin to cause endothelial barrier disruption in acute lung injury.The Journal of biological chemistry · 2023Article
- circEXOC5 promotes acute lung injury through the PTBP1/Skp2/Runx2 axis to activate autophagy.Life science alliance · 2023Article
- Research Progress on Autophagy Regulation by Active Ingredients of Traditional Chinese Medicine in the Treatment of Acute Lung Injury.Journal of inflammation research · 2023Review
- Pulmonary delivery of resveratrol-Drug delivery · 2022Article
- TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury.Heliyon · 2022Article
- Review
- Upregulation ofAnnals of translational medicine · 2022Article
- Knockout of GGPPS1 restrains rab37-mediated autophagy in response to ventilator-induced lung injury.Human cell · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Autophagy is an evolutionarily conserved cellular process that facilitates the continuous recycling of intracellular components (organelles and proteins) and provides an alternative source of energy when nutrients are scarce. Recent studies have implicated autophagy in many disorders, including pulmonary diseases. However, the role of autophagy in endothelial cell (EC) barrier dysfunction and its relevance in the context of acute lung injury (ALI) remain uncertain. Here, we provide evidence that autophagy is a critical component of EC barrier disruption in ALI. Using an aerosolized bacterial lipopolysaccharide (LPS) inhalation mouse model of ALI, we found that administration of the autophagy inhibitor 3-methyladenine (3-MA), either prophylactically or therapeutically, markedly reduced lung vascular leakage and tissue edema. 3-MA was also effective in reducing the levels of proinflammatory mediators and lung neutrophil sequestration induced by LPS. To test the possibility that autophagy in EC could contribute to lung vascular injury, we addressed its role in the mechanism of EC barrier disruption. Knockdown of ATG5, an essential regulator of autophagy, attenuated thrombin-induced EC barrier disruption, confirming the involvement of autophagy in the response. Similarly, exposure of cells to 3-MA, either before or after thrombin, protected against EC barrier dysfunction by inhibiting the cleavage and loss of vascular endothelial cadherin at adherens junctions, as well as formation of actin stress fibers. 3-MA also reversed LPS-induced EC barrier disruption. Together, these data imply a role of autophagy in lung vascular injury and reveal the protective and therapeutic utility of 3-MA against ALI.
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