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Updated: Jan 7, 2026
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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
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Β3-Adrenergic Receptors and Prematurity-Related Diseases: A Systematic Review
Camilla Fazi1,2, Carlo Dani1,2
1Department of Neurosciences, Psychology, Drug Research and Child Health, University of Florence, 50139 Florence, Italy.
Children (Basel, Switzerland)
|December 30, 2025
Summary
Beta3 adrenergic receptors (β3-ARs) are upregulated in hypoxia and may play a role in fetal development and preterm infant diseases. Their activation offers protective effects, but altered expression in preterm infants could contribute to pathologies.
Area of Science:
- Perinatal Medicine
- Molecular Biology
- Developmental Biology
Background:
- Beta3 adrenergic receptors (β3-ARs) exhibit broad tissue expression and diverse functions.
- Emerging research suggests β3-ARs involvement in common preterm infant complications.
- This systematic review investigates the role of β3-ARs in fetal development and neonatal diseases.
Purpose of the Study:
- To systematically review the scientific literature on the association between β3-ARs, fetal development, and diseases in preterm newborns.
Main Methods:
- Searched PubMed/Medline and Cochrane databases for relevant studies.
- Included studies reporting associations between β3-ARs, fetal development, and preterm infant diseases.
- Selected 16 studies from an initial pool of 1596 articles for the review.
Main Results:
- β3-ARs are upregulated in hypoxic conditions across multiple tissues.
- Activation of β3-ARs promotes pro-angiogenic, anti-inflammatory, immunoregulatory, and metabolic adaptation effects.
- These effects are crucial for normal fetal development.
Conclusions:
- Preclinical data indicate a potential role for β3-ARs in the pathogenesis of numerous preterm newborn pathologies.
- Preterm birth disrupts the natural hypoxic fetal environment, exposing infants to relative hyperoxia.
- Altered β3-AR expression and activity due to premature oxygen exposure may impair fetal development and cause organ injury.
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