ArticleBiomolecules2023
β3 Adrenoceptor Agonism Prevents Hyperoxia-Induced Colonic Alterations.
Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- β3-Adrenergic Signaling Preserves Postnatal Maturation of the Enteric Nervous System and Gut Microbiome During Neonatal Hyperoxia.Biomolecules · 2026Article
- HIF1A, ADRB3, and VEGFA gene expression in human cord blood across gestation: insights toward a pharmacological artificial placenta.Pediatric research · 2026Article
- Novel insights into β3-adrenoceptor function in a model of retinopathy of prematurity: the contribution of astrocytes to retinal protection.Frontiers in neuroscience · 2026Article
- Β3-Adrenergic Receptors and Prematurity-Related Diseases: A Systematic Review.Children (Basel, Switzerland) · 2025Review
- βMedicinal research reviews · 2025Review
- Beta-3 Adrenoceptor Agonism Protects the Enteric Nervous Tissue Against Hyperoxia-Induced Damage.Cells · 2025Article
- Emerging opportunities in ROP therapy: from inhibiting pathological vessel growth to promoting physiological vascularization.Frontiers in medicine · 2025Review
- Protective Effects of Beta-3 Adrenoceptor Agonism on Mucosal Integrity in Hyperoxia-Induced Ileal Alterations.Antioxidants (Basel, Switzerland) · 2024Article
- β3-adREnoceptor Analysis in CORD Blood of Neonates (β3 RECORD): Study Protocol of a Pilot Clinical Investigation.Life (Basel, Switzerland) · 2024Article
- Inside the Biology of the β3-Adrenoceptor.Biomolecules · 2024Review
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Oxygen level is a key regulator of organogenesis and its modification in postnatal life alters the maturation process of organs, including the intestine, which do not completely develop in utero. The β3-adrenoreceptor (β3-AR) is expressed in the colon and has an oxygen-dependent regulatory mechanism. This study shows the effects of the β3-AR agonist BRL37344 in a neonatal model of hyperoxia-driven colonic injury. For the first 14 days after birth, Sprague-Dawley rat pups were exposed to ambient oxygen levels (21%) or hyperoxia (85%) and treated daily with BRL37344 at 1, 3, 6 mg/kg or untreated. At the end of day 14, proximal colon samples were collected for analysis. Hyperoxia deeply influences the proximal colon development by reducing β3-AR-expressing cells (27%), colonic length (26%) and mucin production (47%), and altering the neuronal chemical coding in the myenteric plexus without changes in the neuron number. The administration of BRL37344 at 3 mg/kg, but not at 1 mg/kg, significantly prevented these alterations. Conversely, it was ineffective in preventing hyperoxia-induced body weight loss. BRL37344 at 6 mg/kg was toxic. These findings pave the way for β3-AR pharmacological targeting as a therapeutic option for diseases caused by hyperoxia-impaired development, typical prematurity disorders.
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Registered trials
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