ArticleInternational journal of molecular sciences2015
Prenatal exposure to lipopolysaccharide results in myocardial fibrosis in rat offspring.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Structural and Functional Abnormalities in the Preterm Heart: From Development to Adulthood.Journal of the American Heart Association · 2026Review
- The therapeutic potential of zinc-nanoparticles against the cerebellar neurotoxicity induced by bacterial lipopolysaccharides in female rats and their pups.Scientific reports · 2026Article
- Prenatal lipopolysaccharide exposure programs cardiac fibrosis via dysregulating of connexin 43 in offspring rats.Molecular medicine reports · 2026Article
- High-fat intake during lactation ameliorates cardiac fatty acid metabolic disorders and dysfunction in mouse offspring undergoing prenatal poly (I:C) stimulation.Acta pharmacologica Sinica · 2025Article
- Zhilong Huoxue Tongyu capsule alleviates myocardial fibrosis by improving endothelial cell dysfunction.Journal of traditional and complementary medicine · 2024Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- Cardiovascular risk in the postnatal life of children born to women with systemic lupus erythematous.Archivos de cardiologia de Mexico · 2022Article
- Targeting Myadm to Intervene Pulmonary Hypertension on Rats Before Pregnancy Alleviates the Effect on Their Offspring's Cardiac-Cerebral Systems.Frontiers in pharmacology · 2021Article
- Mid-gestation low-dose LPS administration results in female-specific excessive weight gain upon a western style diet in mouse offspring.Scientific reports · 2020Article
- The peptide compound urantide regulates collagen metabolism in atherosclerotic rat hearts and inhibits the JAK2/STAT3 pathway.Molecular medicine reports · 2020Article
- Sex differences in major depression and comorbidity of cardiometabolic disorders: impact of prenatal stress and immune exposures.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Review
- NF-κB-vimentin is involved in steroidogenesis stimulated by di-Toxicology research · 2018Article
- Candidate SNP markers of reproductive potential are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters.BMC genomics · 2018Article
- Prenatal Lipopolysaccharide Exposure Promotes Dyslipidemia in the Male Offspring Rats.Frontiers in physiology · 2018Article
- Prenatal Exposure to Lipopolysaccharide Induces PTX3 Expression and Results in Obesity in Mouse Offspring.Inflammation · 2017Article
- Neonatal Lipopolysaccharide Exposure Gender-Dependently Increases Heart Susceptibility to Ischemia/Reperfusion Injury in Male Rats.International journal of medical sciences · 2017Article
- Sustained elevation of NF-κB activity sensitizes offspring of maternal inflammation to hypertension via impairing PGC-1α recovery.Scientific reports · 2016Article
- Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epigenetic plasticity hypothesis indicates that exposure during pregnancy may cause adult-onset disorders, including hypertension, myocardial infarction and heart failure. Moreover, myocardial fibrosis coincides with hypertension, myocardial infarction and heart failure. This study was designed to investigate the effects of prenatal exposure to lipopolysaccharide (LPS) on myocardial fibrosis. The result showed that at six and 16 weeks of age, the LPS-treated offspring exhibited increased collagen synthesis, an elevated cardiac index (CI), higher mRNA levels of TIMP-2 and TGFβ and a reduced mRNA level of MMP2. The protein levels corresponded to the mRNA levels. The offspring that were prenatally treated with pyrrolidine dithiocarbamic acid (PDTC), an inhibitor of NF-κB, displayed improvements in the CI and in collagen synthesis. Moreover, PDTC ameliorated the expression of cytokines and proteins associated with myocardial fibrosis. The results showed that maternal inflammation can induce myocardial fibrosis in offspring during aging accompanied by an imbalance of TIMP-2/MMP2 and TGFβ expression.
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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.