Association between maternal/newborn genetic variants, placental pathology and spontaneous preterm birth risk: a Romanian population-based study

Preda, Andreia; Caracostea, Gabriela; Ona, Dan; Zaharie, Gabriela; Stamatian, Florin

doi:10.1080/14767058.2018.1517311

Cited by 3 publications

(5 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, some genomic loci have been associated with the gestational duration and PTB risk over the years, as described above. Information from candidate gene studies on inflammatory gene variants associated with an increased PTB risk, from 1999 to date, is listed in Table S1 34–47,49,52–73 . The first gene studied for a possible association with PTB was TNFα , 39 that was followed by other cytokines genes, 35–38,40–47,57,60–66,69,72 MMPs 49,52,56,63,71 and TLRs , 34,62 as previously described.…”

Section: Inflammation In Ptbmentioning

confidence: 99%

“…Besides TLRs , further studies shown the involvement of other immune response‐related genes, such as cytotoxic T‐lymphocyte‐associated protein 4 ( CTLA4 ), 63 monocyte differentiation antigen CD14 ( CD14 ), 63 paraoxonase 2 ( PON2 ), 63 and rFc fragment of IgA receptor ( FcαR ) 65 . Additional genes that are not part of the inflammatory pathway, but were already linked to it, have also been associated with PTB risk, such as genes involved in cell growth, 54,73 vitamin D receptor ( VDR ), 70 coagulation factor V ( F5 ), 55 methylenetetrahydrofolate reductase ( MTHFR ), 58,59,67,68 among others. Overall, 32 genes were linked to PTB risk, and most of the genetic influence is due to maternal variants.…”

Section: Inflammation In Ptbmentioning

confidence: 99%

See 1 more Smart Citation

Inflammatory factors, genetic variants, and predisposition for preterm birth

et al. 2021

View full text Add to dashboard Cite

Preterm birth is a major clinical and public health challenge, with a prevalence of 11% worldwide. It is the leading cause of death in children younger than 5 years old and represents 70% of neonatal deaths and 75% of neonatal morbidity. Despite the clinical and public health significance, this condition's etiology is still unclear, and most of the cases are spontaneous. There are several known preterm birth risk factors, including inflammatory diseases and the genetic background, although the underlying molecular mechanisms are far from understood. The present review highlights the research advances on the association between inflammatory‐related genes and the increased risk for preterm delivery. The most associated genetic variants are the TNFα rs1800629, the IL1α rs17561, and the IL1RN rs2234663. Moreover, many of the genes discussed in this review are also implicated in pathologies involving inflammatory or autoimmune systems, such as periodontal disease, bowel inflammatory disease, and autoimmune rheumatic diseases. This review presents evidence suggesting a common genetic background to preterm birth, autoimmune and inflammatory diseases susceptibility.

show abstract

Section: Inflammation In Ptbmentioning

confidence: 99%

Section: Inflammation In Ptbmentioning

confidence: 99%

Inflammatory factors, genetic variants, and predisposition for preterm birth

et al. 2021

View full text Add to dashboard Cite

show abstract

“…FIRS remains an important issue when we want to refer to the morbidity and prognosis of premature babies, newborns or babies with intrauterine growth restriction, with premature rupture of the membranes (28,29).…”

Section: Discussionmentioning

confidence: 99%

Postpartum assessment of fetal inflammatory response syndrome in a preterm population with premature rupture of membranes: A Romanian study

et al. 2021

Self Cite

View full text Add to dashboard Cite

Fetal inflammatory response syndrome is associated with increased neonatal morbidity and mortality. The aim of the present study was to evaluate the dynamics of the plasmatic value of pro-inflammatory cytokines: tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and neutrophil activating peptide 78 (ENA-78) and the anti-inflammatory cytokine IL-10 in the first and third day of life and the correlation with neonatal morbidities and mortality. The current research was designed as a prospective case control study included 80 neonates hospitalized at the 3rd level Neonatal Intensive Care Unit (NICU),

show abstract

“…SNPs within genes involved in collagen biosynthesis and the synthesis and inhibition of matrix metalloproteases have exhibited associations with PTB [ 68 , 94 – 96 ]. Polymorphisms within genes encoding fibroblast growth factors 1 and 4, both involved in embryonic development, morphogenesis, cell growth, and angiogenesis, have demonstrated associations with sPTB in maternal and infant samples [ 68 , 87 , 97 ]. Genes encoding parturition-related hormones including progesterone, follicle-stimulating hormone, corticotrophin-releasing hormone, and relaxin have also been implicated in candidate genes studies [ 98 – 104 ].…”

Section: Preterm Birth Geneticsmentioning

confidence: 99%

“…Similar findings have been established within PTGS1 , PTGS2 , prostaglandin E receptor 2 ( PTGER2 ), and prostaglandin E receptor 3 ( PTGER3 ) genes in maternal samples and infant samples [ 49 , 69 , 81 , 123 ]. Polymorphisms within genes encoding growth factors involved in vasculogenesis, angiogenesis, endothelin, and endothelial growth have all been implicated in PTB [ 97 , 124 , 125 ]. Potential vascular smooth muscle relaxation via polymorphisms in nitric oxide synthase 2 gene ( NOS2 ) and nitric oxide synthase 3 gene ( NOS3 ) have also been associated with this phenotype [ 118 , 126 ], supporting the role of the vascular and endothelial system in preterm delivery.…”

Section: Preterm Birth Geneticsmentioning

confidence: 99%

The Role of Genetics in Preterm Birth

et al. 2023

View full text Add to dashboard Cite

Preterm birth (PTB), defined as the birth of a child before 37 completed weeks gestation, affects approximately 11% of live births and is the leading cause of death in children under 5 years. PTB is a complex disease with multiple risk factors including genetic variation. Much research has aimed to establish the biological mechanisms underlying PTB often through identification of genetic markers for PTB risk. The objective of this review is to present a comprehensive and updated summary of the published data relating to the field of PTB genetics. A literature search in PubMed was conducted and English studies related to PTB genetics were included. Genetic studies have identified genes within inflammatory, immunological, tissue remodeling, endocrine, metabolic, and vascular pathways that may be involved in PTB. However, a substantial proportion of published data have been largely inconclusive and multiple studies had limited power to detect associations. On the contrary, a few large hypothesis-free approaches have identified and replicated multiple novel variants associated with PTB in different cohorts. Overall, attempts to predict PTB using single “-omics” datasets including genomic, transcriptomic, and epigenomic biomarkers have been mostly unsuccessful and have failed to translate to the clinical setting. Integration of data from multiple “-omics” datasets has yielded the most promising results.

show abstract

Association between maternal/newborn genetic variants, placental pathology and spontaneous preterm birth risk: a Romanian population-based study

Cited by 3 publications

References 38 publications

Inflammatory factors, genetic variants, and predisposition for preterm birth

Inflammatory factors, genetic variants, and predisposition for preterm birth

Postpartum assessment of fetal inflammatory response syndrome in a preterm population with premature rupture of membranes: A Romanian study

The Role of Genetics in Preterm Birth

Contact Info

Product

Resources

About