Background: Preterm delivery (PTD) is the leading cause of neonatal morbidity and mortality. Epidemiologic studies indicate recurrence of PTD is maternally inherited, creating a strong possibility that mitochondrial variants contribute to its etiology. This study examines the association between mitochondrial genotypes and PTD and related outcomes.
Methods: This study combined, through meta-analysis, two case-control, genome-wide association studies: one from the Danish National Birth Cohort Study and one from the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health. The outcomes of PTD (≤36 wk), very PTD (≤32 wk), and preterm prelabor rupture of membranes (PPROM) were examined. A total of 135 individual single-nucleotide polymorphism (SNP) associations were tested using the combined genome from mothers and neonates (case vs. control) in each population and then pooled via meta-analysis.
Results: After meta-analysis, there were four SNPs for the outcome of PTD below P ≤ 0.10 and two below P ≤ 0.05. For the additional outcomes of very PTD and PPROM, there were three and four SNPs, respectively, below P ≤ 0.10.
Conclusion: Given the number of tests, no single SNP reached study-wide significance (P = 0.0006). Our study does not support the hypothesis that mitochondrial genetics contributes to the maternal transmission of PTD and related outcomes.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694399 | PMC |
| http://dx.doi.org/10.1038/pr.2012.112 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Epigenetic memory as crucial contributing factor in directing the differentiation of human iPSC into pancreatic β-cells in vitro.
Cell Tissue Res
January 2025
Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Qatar Foundation (QF), Hamad Bin Khalifa University (HBKU), Doha, Qatar.
Impaired insulin secretion contributes to the pathogenesis of type 1 diabetes mellitus through autoimmune destruction of pancreatic β-cells and the pathogenesis of severe forms of type 2 diabetes mellitus through β-cell dedifferentiation and other mechanisms. Replenishment of malfunctioning β-cells via islet transplantation has the potential to induce long-term glycemic control in the body. However, this treatment option cannot widely be implemented in clinical due to healthy islet donor shortage.
View Article and Find Full Text PDFPolystyrene Nanoplastics Hitch-Hike the Gut-Brain Axis to Exacerbate Parkinson's Pathology.
ACS Nano
January 2025
Nanomedicine Center, The Great Bay Area National Institute for Nanotechnology Innovation, 136 Kaiyuan Avenue, Guangzhou 510700, China.
The neurological implications of micro- and nanoplastic exposure have recently come under scrutiny due to the environmental prevalence of these synthetic materials. Parkinson's disease (PD) is a major neurological disorder clinically characterized by intracellular Lewy-body inclusions and dopaminergic neuronal death. These pathological hallmarks of PD, according to Braak's hypothesis, are mediated by the afferent propagation of α synuclein (αS) via the enteric nervous system, or the so-called gut-brain axis.
View Article and Find Full Text PDFSupplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage.
Metabol Open
March 2025
Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, 3886, South Africa.
Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used to assess the pharmacological effect of drugs, were pretreated with the dietary compounds, aspalathin (1 μM) and sulforaphane (10 μM) before exposure to palmitic acid (0.
View Article and Find Full Text PDFChronic fetal hypoxia and antenatal Vitamin C exposure differentially regulate molecular signalling in the lung of female lambs in early adulthood.
Front Physiol
January 2025
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom.
Introduction: Chronic fetal hypoxia is commonly associated with fetal growth restriction and can predispose to respiratory disease at birth and in later life. Antenatal antioxidant treatment has been investigated to overcome the effects of oxidative stress to improve respiratory outcomes. We aimed to determine if the effects of chronic fetal hypoxia and antenatal antioxidant administration persist in the lung in early adulthood.
View Article and Find Full Text PDFRemodeling of ER Membrane Contact Sites During Cell Division.
Contact (Thousand Oaks)
January 2025
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Doha, Qatar.
Membrane contact sites (MCS) provide specialized conduits for inter-organelle communications to maintain cellular homeostasis. Most organelles are interconnected, which supports their coordination and function. M-phase (mitosis or meiosis) is associated with dramatic cellular remodeling to support cell division, including the equal distribution of organelles to the two daughter cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!