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A poorly functioning placenta results in impaired exchanges of oxygen, nutrition, wastes and hormones between the mother and her fetus. This can lead to restriction of fetal growth. These growth restricted babies are at increased risk of developing chronic diseases, such as type-2 diabetes, hypertension, and kidney disease, later in life. Animal studies have shown that growth restricted phenotypes are sex-dependent and can be transmitted to subsequent generations through both the paternal and maternal lineages. Altered epigenetic mechanisms, specifically changes in DNA methylation, histone modifications, and non-coding RNAs that regulate expression of genes that are important for fetal development have been shown to be associated with the transmission pattern of growth restricted phenotypes. This review will discuss the subsequent health outcomes in the offspring after growth restriction and the transmission patterns of these diseases. Evidence of altered epigenetic mechanisms in association with fetal growth restriction will also be reviewed.
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http://dx.doi.org/10.3389/fendo.2022.838737 | DOI Listing |
Elife
September 2025
Center for Autoimmune Genomics and Etiology, Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Human cytomegalovirus (HCMV) infects up to 80% of the world's population. Here, we show that HCMV infection leads to widespread changes in human chromatin accessibility and chromatin looping, with hundreds of thousands of genomic regions affected 48 hr after infection. Integrative analyses reveal HCMV-induced perturbation of Hippo signaling through drastic reduction of TEAD1 transcription factor activity.
View Article and Find Full Text PDFJ Oral Pathol Med
September 2025
Department of Oral and Maxillofacial Pathology, Federal University of Uberlândia, Uberlândia, Minas Gerais, Brazil.
Background: Oral squamous cell carcinoma (OSCC) is one of the most frequent head and neck cancers. The 4-nitroquinoline 1-oxide (4NQO) mouse model of oral carcinogenesis is a well-established model to investigate the mechanism behind OSCC development, including epigenetic alterations. Studies have shown that histone acetylation is a key regulator of gene expression and may play a role in such a tumor.
View Article and Find Full Text PDFNanotoxicology
September 2025
Department of Biophysics of Environmental Pollution, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
The effect of non-functionalized polystyrene nanoparticles (PS-NPs) with diameters of 29, 44, and 72 nm on plasmid DNA integrity and the expression of genes involved in the architecture of chromatin was investigated in human peripheral blood mononuclear cells (PBMCs). The cells were incubated with PS-NPs at concentrations ranging from 0.001 to 100 µg/mL for 24 hours.
View Article and Find Full Text PDFFront Immunol
September 2025
Precision Pharmacy and Drug Development Center, Department of Pharmacy, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Gliomas are the most common primary malignant tumors of the central nervous system (CNS), and despite progress in molecular diagnostics and targeted therapies, their prognosis remains poor. In recent years, immunotherapy has emerged as a promising treatment modality in cancer therapy. However, the inevitable immune evasion by tumor cells is a key barrier affecting therapeutic efficacy.
View Article and Find Full Text PDFClin Kidney J
September 2025
Department of Nephrology. University Clinical Hospital, INCLIVA, Valencia. RICORS Renal Instituto de salud Carlos III, Valencia. Spain.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major contributor to systemic metabolic dysfunction and is increasingly recognized as a risk enhancer for both cardiovascular disease (CVD) and chronic kidney disease (CKD). This review explores the complex interconnections between MASLD, CVD, and CKD, with emphasis on shared pathophysiological mechanisms and the clinical implications for risk assessment and management. We describe the crosstalk among the liver, heart, and kidneys, focusing on insulin resistance, chronic inflammation, and progressive fibrosis as key mediators.
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