ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Metformin-stimulated AMPK-α1 promotes microvascular repair in acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.
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Who cites it
52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.
- Diabetes Mellitus and COVID-19 in Adults: A Systematic Review of Pathophysiological Connections, Clinical Outcomes, and Therapeutic Considerations.International journal of molecular sciences · 2026Pooled it
- Effects of metformin on acute respiratory distress syndrome in preclinical studies: a systematic review and meta-analysis.Frontiers in pharmacology · 2023Pooled it
- DRD1 downregulation contributes to mechanical stretch-induced lung endothelial barrier dysfunction.Theranostics · 2021Trial
- Metformin attenuates lung ischemia-reperfusion injury and necroptosis through AMPK pathway in type 2 diabetic recipient rats.BMC pulmonary medicine · 2024Article
- Anti-Inflammatory Potential of the Anti-Diabetic Drug Metformin in the Prevention of Inflammatory Complications and Infectious Diseases Including COVID-19: A Narrative Review.International journal of molecular sciences · 2024Review
- Targeting AMP-activated protein kinase in sepsis.Frontiers in endocrinology · 2024Review
- The Apelin/APJ System: A Potential Therapeutic Target for Sepsis.Journal of inflammation research · 2024Review
- AMPK activation improves recovery from pneumonia-induced lung injury via reduction of er-stress and apoptosis in alveolar epithelial cells.Respiratory research · 2023Article
- Rapamycin prevents lung injury related to acute spinal cord injury in rats.Scientific reports · 2023Article
- COVID-19: Diabetes Perspective-Pathophysiology and Management.Pathogens (Basel, Switzerland) · 2023Review
- Metformin alleviates lung-endothelial hyperpermeability by regulating cofilin-1/PP2AC pathway.Frontiers in pharmacology · 2023Article
- FJU-C28 inhibits the endotoxin-induced pro-inflammatory cytokines expression via suppressing JNK, p38 MAPK and NF-κB signaling pathways.Pharmacology research & perspectives · 2021Article
- AICAR decreases acute lung injury by phosphorylating AMPK and upregulating heme oxygenase-1.The European respiratory journal · 2021Article
- Diabetes mellitus and COVID-19: Understanding the association in light of current evidence.World journal of clinical cases · 2021Review
- Metformin acts to suppress β-hydroxybutyric acid-mediated inflammatory responses through activation of AMPK signaling in bovine hepatocytes.Journal of animal science · 2021Article
- Canagliflozin protects against sepsis capillary leak syndrome by activating endothelial α1AMPK.Scientific reports · 2021Article
- Adipose-derived stem cells combined with platelet-rich plasma enhance wound healing in a rat model of full-thickness skin defects.Stem cell research & therapy · 2021Article
- Dietary Control of Inflammation and Resolution.Frontiers in nutrition · 2021Review
- Repurposing existing drugs for COVID-19: an endocrinology perspective.BMC endocrine disorders · 2020Article
- α1AMP-Activated Protein Kinase Protects against Lipopolysaccharide-Induced Endothelial Barrier Disruption via Junctional Reinforcement and Activation of the p38 MAPK/HSP27 Pathway.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Acute lung injury secondary to sepsis is a leading cause of mortality in sepsis-related death. Present therapies are not effective in reversing endothelial cell dysfunction, which plays a key role in increased vascular permeability and compromised lung function. AMP-activated protein kinase (AMPK) is a molecular sensor important for detection and mediation of cellular adaptations to vascular disruptive stimuli. In this study, we sought to determine the role of AMPK in resolving increased endothelial permeability in the sepsis-injured lung. AMPK function was determined in vivo using a rat model of endotoxin-induced lung injury, ex vivo using the isolated lung, and in vitro using cultured rat pulmonary microvascular endothelial cells (PMVECs). AMPK stimulation using N1-(α-d-ribofuranosyl)-5-aminoimidizole-4-carboxamide or metformin decreased the LPS-induced increase in permeability, as determined by filtration coefficient (Kf) measurements, and resolved edema as indicated by decreased wet-to-dry ratios. The role of AMPK in the endothelial response to LPS was determined by shRNA designed to decrease expression of the AMPK-α1 isoform in capillary endothelial cells. Permeability, wounding, and barrier resistance assays using PMVECs identified AMPK-α1 as the molecule responsible for the beneficial effects of AMPK in the lung. Our findings provide novel evidence for AMPK-α1 as a vascular repair mechanism important in the pulmonary response to sepsis and identify a role for metformin treatment in the management of capillary injury.
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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.