Evidence map›Paper›PMID 42150845›Full record

Observational studyBMJ paediatrics open2026

Autophagy markers in umbilical cord blood-derived PBMCs and their association with preterm morbidities: a prospective multicenter cohort study.

Coşkun Armağan, Can Akyıldız, Gizem Bakır, Tuğba Üçüncü Egeli, Beyza Türe, Funda Erdoğan, Bora Taştan, Defne Engür, Özgür Olukman, Sümer Sütçüoğlu and 6 more

Abstract readMulticenter StudyObservational Study
In one paragraph

Observational study in BMJ paediatrics open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Coşkun ArmağanFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0001-9716-130X
Can AkyıldızFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0002-7087-7006
Gizem BakırDepartment of Pediatric Endocrinology, Ankara Etlik City Hospital, University of Health Sciences, Ankara, Turkey.ORCID http://orcid.org/0000-0002-8594-4777
Tuğba Üçüncü EgeliFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0003-1014-4852
Beyza TüreIzmir International Biomedicine and Genome Institute, Dokuz Eylul University, İzmir, Turkey.ORCID http://orcid.org/0009-0003-1239-8917
Funda ErdoğanFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0001-5348-1168
Bora TaştanIzmir International Biomedicine and Genome Institute, Dokuz Eylul University, İzmir, Turkey.ORCID http://orcid.org/0000-0001-6189-7227
Defne EngürIzmir Tepecı̇k Education and Research Hospital, Department of Pediatrics, Division of Neonatology, University of Health Sciences, İzmir, Turkey.ORCID http://orcid.org/0000-0003-0405-085X
Özgür OlukmanÇı̇ğlı̇ Education and Research Hospital, Department of Pediatrics, Division of Neonatology, Bakırçay University, İzmir, Turkey.ORCID http://orcid.org/0000-0003-4006-0465
Sümer SütçüoğluIzmir Tepecı̇k Education and Research Hospital, Department of Pediatrics, Division of Neonatology, University of Health Sciences, İzmir, Turkey.ORCID http://orcid.org/0000-0002-9598-1993
Özgün UygurIzmir Tepecı̇k Education and Research Hospital, Department of Pediatrics, Division of Neonatology, University of Health Sciences, İzmir, Turkey.ORCID http://orcid.org/0000-0002-7580-915X
Deniz GonülalIzmir Tepecı̇k Education and Research Hospital, Department of Pediatrics, Division of Neonatology, University of Health Sciences, İzmir, Turkey.ORCID http://orcid.org/0000-0002-9816-0613
Burak DeliloğluFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0002-1914-6099
Nuray DumanFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey.ORCID http://orcid.org/0000-0003-0545-2914
Şermin GençIzmir International Biomedicine and Genome Institute, Dokuz Eylul University, İzmir, Turkey.ORCID http://orcid.org/0000-0001-6126-7460
Hasan ÖzkanFaculty of Medicine, Department of Pediatrics, Division of Neonatology, Dokuz Eylül University, İzmir, Turkey hozkandeu@gmail.com.ORCID http://orcid.org/0000-0003-2542-7441

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAutophagy is a crucial cellular degradation pathway that maintains homeostasis during stress. Preterm infants are exposed to significant oxidative and metabolic stress during the perinatal transition. This study aimed to evaluate the levels of autophagy markers (Beclin-1, LC3B-I and LC3B-II) in the umbilical cord blood of preterm infants and investigate their association with neonatal morbidities and mortality. MATERIAL AND

methodsThis prospective multicentre cohort study included 60 preterm infants. Umbilical cord blood samples were analysed for Beclin-1, LC3B-I and LC3B-II levels using Western blot. The LC3B-I/LC3B-II ratio was calculated as an indicator of autophagic flux. The relationship between these markers and major neonatal outcomes (respiratory distress syndrome (RDS), intraventricular haemorrhage (IVH), haemodynamically significant patent ductus arteriosus (hsPDA), early neonatal sepsis (ENS) and mortality) was evaluated using Mann-Whitney U tests and multivariable logistic regression adjusted for gestational age.

resultsA significant positive correlation was observed between gestational age and Beclin-1 levels (r=0.406, p=0.005). In subgroup analyses, non-survivors exhibited significantly lower median Beclin-1 levels (0.45 vs 0.92, p=0.047) and a depressed LC3B-I/LC3B-II ratio (0.48 vs 1.90, p=0.018) compared with survivors. Similarly, infants with IVH had significantly lower LC3B-I levels (0.07 vs 0.65, p=0.011). However, in multivariable logistic regression analyses adjusted for gestational age, the independent statistical significance of these markers was attenuated, suggesting that the observed autophagic impairment is closely linked to gestational immaturity. No significant associations were found for RDS, hsPDA or ENS. DISCUSSION: This study identifies lower cord blood Beclin-1 levels and an altered LC3B ratio as potential markers of vulnerability in preterm infants, particularly for mortality and IVH. The findings suggest that autophagic capacity at birth is developmentally regulated, with more immature infants displaying compromised autophagy initiation.

Indexed as

AutophagyBeclin-1Fetal BloodInfant, Premature, DiseasesMicrotubule-Associated ProteinsBiomarkersFemaleGestational AgeHumansInfant, NewbornInfant, PrematureMaleProspective StudiesBeclin-1BECN1 protein, humanBiomarkersMAP1LC3B protein, humanMicrotubule-Associated ProteinsIntensive Care Units, NeonatalNeonatology

Identifiers

PMID42150845
PMCPMC13185041

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.