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Updated: Jul 20, 2026

Transcutaneous Microcirculatory Imaging in Preterm Neonates
Published on: December 31, 2015
Differences in autophagy marker levels at birth in preterm vs. term infants
Noëmi Künstle1,2, Olga Gorlanova1, Andrea Marten1
1University Children's Hospital Basel UKBB, University of Basel, Basel, Switzerland.
Autophagy markers differ in preterm infants, with higher p62 and lower SIRT1 levels, potentially linked to impaired oxidative stress response and lung development. This study highlights differences in autophagy in preterm infants, impacting respiratory health.
Area of Science:
- Neonatal Medicine
- Cellular Biology
- Respiratory Medicine
Background:
- Preterm infants face increased oxidative stress and respiratory risks.
- Autophagy is crucial for cellular defense against oxidative damage and lung development.
- Autophagy's role in preterm infants' respiratory health is understudied.
Purpose of the Study:
- To investigate differences in autophagy marker levels between preterm and term infants.
- To explore the association of autophagy markers with gestational age in newborns.
Main Methods:
- Prospective study of the Basel-Bern Infant Lung Development (BILD) cohort.
- Comparison of cord blood levels of macroautophagy (Beclin-1, LC3B), selective autophagy (p62), and autophagy regulation (SIRT1).
- Analysis included 64 preterm and 453 term infants.
Main Results:
- Beclin-1 and LC3B levels did not differ between preterm and term infants.
- Preterm infants showed higher p62 and lower SIRT1 levels in cord blood.
- p62 levels decreased, while SIRT1 levels increased with advancing gestational age.
Conclusions:
- Key autophagy markers exhibit differential levels in preterm versus term infants.
- Findings suggest a link between altered autophagy, impaired oxidative stress response, and lung development in preterm infants.
- This study provides foundational insights into autophagy mechanisms in preterm neonates and their potential association with respiratory morbidity.
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