ArticleNature communications2022
Maternal and perinatal obesity induce bronchial obstruction and pulmonary hypertension via IL-6-FoxO1-axis in later life.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Mesenchyme-derived inflammation during the saccular stage recruits macrophages and alters lung development.JCI insight · 2026Article
- The autonomic nervous system-lung interface in experimental BPD: NPY modulates immune response, alveolar growth and vascular muscularizationin neonatal mice exposed to oxidative stress.Respiratory research · 2026Article
- Prenatal non-infectious mild stressor modulates early-life lung development in a time-specific manner.Respiratory research · 2026Article
- Paternal sleep deprivation and cardiac dysfunction in offspring: A perspective of myocardial hypertrophy.Experimental physiology · 2026Article
- Lipid Metabolism and Obesity in Early Life: Drivers of Chronic Lung Disease From Development to Adulthood.Molecular nutrition & food research · 2026Review
- Targeting IL6-Edn1-FoxO1 axis enables lung growth in mechanically ventilated newborn mice.The European respiratory journal · 2025Article
- New insights into pulmonary arterial hypertension: interaction between PANoptosis and perivascular inflammatory responses.Apoptosis : an international journal on programmed cell death · 2025Review
- Perinatal obesity primes the hepatic metabolic stress response in the offspring across life span.Scientific reports · 2025Article
- Advances in Interleukin-6 Family Cytokines and the Role in Respiratory Diseases.Journal of inflammation research · 2025Review
- The Role of Early Child Nutrition in Pulmonary Hypertension-A Narrative Review.Children (Basel, Switzerland) · 2024Review
- Seeing pulmonary hypertension through a paediatric lens: a viewpoint.The European respiratory journal · 2024Article
- Identification of related-genes of T cells in lung tissue of chronic obstructive pulmonary disease based on bioinformatics and experimental validation.Scientific reports · 2024Article
- The importance of translational science within the respiratory field.Breathe (Sheffield, England) · 2024Article
- ERS International Congress 2023: highlights from the Paediatrics Assembly.ERJ open research · 2024Article
- CXCL10 deficiency limits macrophage infiltration, preserves lung matrix, and enables lung growth in bronchopulmonary dysplasia.Inflammation and regeneration · 2023Article
- Characterizing and Quenching Autofluorescence in Fixed Mouse Adrenal Cortex Tissue.International journal of molecular sciences · 2023Article
- Perinatal Obesity Sensitizes for Premature Kidney Aging Signaling.International journal of molecular sciences · 2023Article
- Endothelial cell clonality, heterogeneity and dysfunction in pulmonary arterial hypertension.Frontiers in medicine · 2023Review
- Review
- Maternal and perinatal obesity induce bronchial obstruction and pulmonary hypertension via IL-6-FoxO1-axis in later life.Nature communications · 2022Article
Corrections and comments
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Authors and funding
26 authors at 7 institutions in 3 countries.
Funding
Abstract
Obesity is a pre-disposing condition for chronic obstructive pulmonary disease, asthma, and pulmonary arterial hypertension. Accumulating evidence suggests that metabolic influences during development can determine chronic lung diseases (CLD). We demonstrate that maternal obesity causes early metabolic disorder in the offspring. Here, interleukin-6 induced bronchial and microvascular smooth muscle cell (SMC) hyperproliferation and increased airway and pulmonary vascular resistance. The key anti-proliferative transcription factor FoxO1 was inactivated via nuclear exclusion. These findings were confirmed using primary SMC treated with interleukin-6 and pharmacological FoxO1 inhibition as well as genetic FoxO1 ablation and constitutive activation. In vivo, we reproduced the structural and functional alterations in offspring of obese dams via the SMC-specific ablation of FoxO1. The reconstitution of FoxO1 using IL-6-deficient mice and pharmacological treatment did not protect against metabolic disorder but prevented SMC hyperproliferation. In human observational studies, childhood obesity was associated with reduced forced expiratory volume in 1 s/forced vital capacity ratio Z-score (used as proxy for lung function) and asthma. We conclude that the interleukin-6-FoxO1 pathway in SMC is a molecular mechanism by which perinatal obesity programs the bronchial and vascular structure and function, thereby driving CLD development. Thus, FoxO1 reconstitution provides a potential therapeutic option for preventing this metabolic programming of CLD.
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Registered trials
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