ArticleFrontiers in cell and developmental biology2022
Paternal alcohol exposures program intergenerational hormetic effects on offspring fetoplacental growth.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review on the role of paternal factors in human placental development, function, and pregnancy-related disorders.Journal of assisted reproduction and genetics · 2025Pooled it
- Preconception Chronic Intermittent Ethanol Exposure Impacts Offspring Transcriptomes with Sex and Tissue Specific Effects.bioRxiv : the preprint server for biology · 2026Article
- Maternal, paternal, and dual-parental alcohol exposures result in both overlapping and distinct impacts on behavior in adolescent offspring.Alcohol (Fayetteville, N.Y.) · 2025Article
- Preconception Paternal Alcohol Consumption Elicits Postnatal Changes in Neural Retinas of the Offspring.Investigative ophthalmology & visual science · 2025Article
- Nonconceptus Mechanisms of Prenatal Alcohol Exposure That Disrupt Embryo-Fetal Development: An Integrative View.Alcohol research : current reviews · 2025Review
- Therapy to teratology: chronic paternal antioxidant supplementation alters offspring placental architecture and craniofacial morphogenesis in a mouse model.Frontiers in cell and developmental biology · 2025Article
- Parental Alcohol Exposures Associate with Lasting Mitochondrial Dysfunction and Accelerated Aging in a Mouse Model.Aging and disease · 2024Article
- Alterations in sperm RNAs persist after alcohol cessation and correlate with epididymal mitochondrial dysfunction.Andrology · 2024Article
- Clinical Diagnosis and Management of Fetal Alcohol Spectrum Disorder and Sensory Processing Disorder in Children.Children (Basel, Switzerland) · 2024Review
- Unveiling the hidden risk: paternal smoking and alcohol exposure prior to conception as independent factors for allergic rhinitis in children.Frontiers in pediatrics · 2024Article
- Chronic paternal alcohol exposures induce dose-dependent changes in offspring craniofacial shape and symmetry.Frontiers in cell and developmental biology · 2024Article
- Teratogenesis and the epigenetic programming of congenital defects: Why paternal exposures matter.Birth defects research · 2023Review
- Preconception paternal alcohol exposure decreases IVF embryo survival and pregnancy success rates in a mouse model.Molecular human reproduction · 2023Article
- Prenatal paternal anxiety symptoms predict child DHEA levels and internalizing symptoms during adrenarche.Frontiers in behavioral neuroscience · 2023Article
- Paternal epigenetic influences on placental health and their impacts on offspring development and disease.Frontiers in genetics · 2022Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Hormesis refers to graded adaptive responses to harmful environmental stimuli where low-level toxicant exposures stimulate tissue growth and responsiveness while, in contrast, higher-level exposures induce toxicity. Although the intergenerational inheritance of programmed hormetic growth responses is described in plants and insects, researchers have yet to observe this phenomenon in mammals. Using a physiologically relevant mouse model, we demonstrate that chronic preconception paternal alcohol exposures program nonlinear, dose-dependent changes in offspring fetoplacental growth. Our studies identify an inverse j-shaped curve with a threshold of 2.4 g/Kg per day; below this threshold, paternal ethanol exposures induce programmed increases in placental growth, while doses exceeding this point yield comparative decreases in placental growth. In male offspring, higher paternal exposures induce dose-dependent increases in the placental labyrinth layer but do not impact fetal growth. In contrast, the placental hypertrophy induced by low-level paternal ethanol exposures associate with increased offspring crown-rump length, particularly in male offspring. Finally, alterations in placental physiology correlate with disruptions in both mitochondrial-encoded and imprinted gene expression. Understanding the influence of ethanol on the paternally-inherited epigenetic program and downstream hormetic responses in offspring growth may help explain the enormous variation observed in fetal alcohol spectrum disorder (FASD) phenotypes and incidence.
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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 Socratic graph.