ArticlePediatric research2019
MIF inhibition enhances pulmonary angiogenesis and lung development in congenital diaphragmatic hernia.
Article in Pediatric research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Toll-like receptors ligand immunomodulators for the treatment congenital diaphragmatic hernia.Orphanet journal of rare diseases · 2024Article
- Congenital diaphragmatic hernia: phosphodiesterase-5 and Arginase inhibitors prevent pulmonary vascular hypoplasia in rat lungs.Pediatric research · 2024Article
- MIF Increases sFLT1 Expression in Early Uncomplicated Pregnancy and Preeclampsia.International journal of molecular sciences · 2023Article
- Establishment of tissue-resident immune populations in the fetus.Seminars in immunopathology · 2022Review
- Emerging antenatal therapies for congenital diaphragmatic hernia-induced pulmonary hypertension in preclinical models.Pediatric research · 2021Review
- Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage.Nature communications · 2021Article
- Honeymoon Period in Newborn Rats With CDH Is Associated With Changes in the VEGF Signaling Pathway.Frontiers in pediatrics · 2021Article
- Macrophage migration inhibitory factor (MIF) in the development and progression of pulmonary arterial hypertension.Global cardiology science & practice · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCongenital diaphragmatic hernia (CDH) is a complex birth anomaly with significant mortality and morbidity. Lung hypoplasia and persistent pulmonary hypertension (PPHN) limit survival in CDH. Macrophage migration inhibitory factor (MIF), a key regulator of innate immunity, is involved in hypoxia-induced vascular remodeling and PPHN. We hypothesized that antenatal inhibition of MIF in CDH fetuses, would reduce vascular remodeling, and improve angiogenesis and lung development.
methodsPregnant rats were randomized into three groups: Control, nitrofen, and nitrofen + ISO-92. Lung volumes of pups were measured by CT scanning. Right ventricular systolic pressure (RVSP) and vascular wall thickness (VWT) were measured together with MIF concentration, angiogenesis markers, lung morphometry, and histology.
resultsPrenatal treatment with ISO-92, an MIF inhibitor, improved normalization of static lung volume, lung volume-to-body weight ratio, decreased alveolar septal thickness, RVSP and VWT and improved radial alveolar count as compared to the non-treated group. Expression of MIF was unaffected by ISO-92; however, ISO-92 increased p-eNOS and VEGF activities and reduced arginase 1, 2 and Sflt-1.
conclusionPrenatal inhibition of MIF activity in CDH rat model improves angiogenesis and lung development. This selective intervention may be a future therapeutic strategy to reduce the morbidity and mortality of this devastating condition.
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