ArticleMolecular and cellular biology2011
Increased Akt-mTOR signaling in lung epithelium is associated with respiratory distress syndrome in mice.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Lipid Metabolism and Obesity in Early Life: Drivers of Chronic Lung Disease From Development to Adulthood.Molecular nutrition & food research · 2026Review
- Unraveling the Impact ofLife (Basel, Switzerland) · 2024Article
- SIRT1 alleviates insulin resistance and respiratory distress in late preterm rats by activating QKI5-mediated PPARγ/PI3K/AKT pathway.Cell cycle (Georgetown, Tex.) · 2023Article
- Reticulons 1 and 3 are essential for axonal growth and synaptic maintenance associated with intellectual development.Human molecular genetics · 2023Article
- The Role of Autophagy in Lamellar Body Formation and Surfactant Production in Type 2 Alveolar Epithelial Cells.International journal of biological sciences · 2022Article
- mTORC1 is a mechanosensor that regulates surfactant function and lung compliance during ventilator-induced lung injury.JCI insight · 2021Article
- Molecular Mechanisms of Maternal Diabetes Effects on Fetal and Neonatal Surfactant.Children (Basel, Switzerland) · 2021Review
- Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases.Frontiers in medicine · 2021Review
- Protective effect of a mechanistic target of rapamycin inhibitor on an in vivo model ofcisplatin-induced ovarian gonadotoxicity.Experimental animals · 2018Article
- Early injury of the neonatal lung contributes to premature lung aging: a hypothesis.Molecular and cellular pediatrics · 2016Review
- Consequences of a Maternal High-Fat Diet and Late Gestation Diabetes on the Developing Rat Lung.PloS one · 2016Article
- Differential expression of GSK3β and pS9GSK3β in normal human tissues: can pS9GSK3β be an epithelial marker?International journal of clinical and experimental pathology · 2015Article
- Administration of antenatal glucocorticoids and postnatal surfactant ameliorates respiratory distress syndrome-associated neonatal lethality in Erk3(-/-) mouse pups.Pediatric research · 2014Article
- Hypoxia induces permeability and giant cell responses of Andes virus-infected pulmonary endothelial cells by activating the mTOR-S6K signaling pathway.Journal of virology · 2013Article
- Deficiency in pulmonary surfactant proteins in mice with fatty acid binding protein 4-Cre-mediated knockout of the tuberous sclerosis complex 1 gene.Experimental physiology · 2013Article
- Insulin and the lung: connecting asthma and metabolic syndrome.Journal of allergy · 2013Review
- Andes virus infection of lymphatic endothelial cells causes giant cell and enhanced permeability responses that are rapamycin and vascular endothelial growth factor C sensitive.Journal of virology · 2012Article
- VEGF levels in humans and animal models with RDS and BPD: temporal relationships.Experimental lung research · 2012Review
- Care of the infant of the diabetic mother.Current diabetes reports · 2012Review
- Activation of hypoxia-inducible factor-1 protects airway epithelium against oxidant-induced barrier dysfunction.American journal of physiology. Lung cellular and molecular physiology · 2011Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pregnancy in women with diabetes is associated with a higher risk of perinatal complications. In particular, infants of diabetic mothers frequently suffer from respiratory distress syndrome (RDS), which is a leading cause of death in preterm infants and is considered to be primarily due to hyperinsulinemia in infants in response to maternal hyperglycemia. To elucidate the mechanism of how insulin signaling induces RDS, bronchoalveolar epithelium-specific Akt1 transgenic (TG) mice were generated. Akt1 overexpression in fetal lung epithelium resulted in RDS in preterm infants born by Caesarean section at embryonic day 18.5 (E18.5). The expression levels of hypoxia-inducible factor 2α (HIF-2α) and its target vascular endothelial growth factor (VEGF) were downregulated in the lung of Akt1 TG mice. Inhibition of the Akt-mammalian target of rapamycin (mTOR) signaling axis by rapamycin restored the expression of VEGF and improved the lung pathology of Akt1 TG pups. Rapamycin also attenuated the RDS phenotype in wild-type mice delivered preterm at E17.5. In cultured lung epithelial cells, insulin reduced VEGF expression and transcriptional activity of HIF-2 on VEGF promoter in an mTOR-dependent manner. Thus, aberrant activation of the Akt-mTOR pathway in lung epithelium plays a causal role in the pathogenesis of infant RDS, presumably through downregulation of HIF-2-dependent VEGF expression in the lung.
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