ArticlePediatric research2026
Individual and joint association of maternal and cord blood mitochondrial DNA heteroplasmy and copy number with preterm birth.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundThe biological mechanisms underlying preterm birth (PTB) are not fully understood. This study examined the individual and joint associations of mitochondrial DNA (mtDNA) heteroplasmy and copy number (mtDNA-CN) in maternal and cord blood with PTB.
methodsThis study analyzed 998 mother-infant dyads (18% PTB). MtDNA heteroplasmy and mtDNA-CN were measured by a targeted DNA sequencing approach using umbilical cord blood collected at birth and maternal blood collected 24-72 hours postpartum. Multivariable logistic regressions were used to evaluate the associations with PTB.
resultsMaternal predicted pathogenic heteroplasmy was associated with a twofold increased risk of PTB (adjusted OR (95% CI) = 2.08 (1.07, 4.05)), whereas no significant associations were observed for maternal overall or functional heteroplasmy. No significant associations were observed for cord blood heteroplasmy measures. A U-shaped association between maternal mtDNA-CN and PTB was observed. Higher cord mtDNA-CN were associated with increased PTB odds (1.36 (1.14, 1.62)). Notably, a significant interaction between maternal and cord mtDNA-CN was found for PTB risk.
conclusionMaternal, but not fetal, mtDNA heteroplasmy was associated with increased PTB risk. Both maternal and cord blood mtDNA-CN demonstrated individual and interactive associations with PTB, suggesting that maternal and fetal mitochondrial genomic variations may jointly influence PTB risk. IMPACT: We found that maternal predicted pathogenic mtDNA heteroplasmy was associated with increased PTB risk; maternal mtDNA-CN showed a U-shaped association with PTB; and higher cord blood mtDNA-CN was positively associated with PTB. This study provides the first evidence from a large birth cohort simultaneously assessing maternal and fetal mtDNA heteroplasmy and mtDNA-CN in relation to PTB, adding a mitochondrial genetics perspective to PTB research. This study highlights mitochondrial genomic variation as a novel pathway in PTB pathogenesis and suggests the potential utility of mtDNA measures as biomarkers for early risk assessment and as a basis for future mitochondria-targeted interventions.
Identifiers
What OpenQuestion holds
Registered trials
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.