ReviewFrontiers in endocrinology2021
Dimming the Powerhouse: Mitochondrial Dysfunction in the Liver and Skeletal Muscle of Intrauterine Growth Restricted Fetuses.
Review in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- The Interplay of One-Carbon Metabolism, Mitochondrial Function, and Developmental Programming in Ruminant Livestock.Journal of developmental biology · 2026Review
- When bovine life begins in a petri dish: transcriptomic insights from embryos to calves conceived in vitro.The Journal of reproduction and development · 2026Review
- Metabolic Reprogramming of Oligodendrocytes in Intrauterine Growth Restriction.Developmental neuroscience · 2026Article
- Integrated metabolomics and computational analysis suggest that aFrontiers in nutrition · 2026Article
- Slow-twitch oxidative myofiber proportions and capillary number per myofiber are reduced in growth-restricted fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Insights into the Hepatic Arterial Buffer Response in Late-Onset FGR.Journal of clinical medicine · 2025Article
- Developmental regulation of fetal mitochondrial respiratory function towards term: the role of glucocorticoid and thyroid hormones.The Journal of endocrinology · 2025Review
- Fetal programming under maternal heat stress: a focus on skeletal muscle growth and nutrition in livestock.Journal of developmental origins of health and disease · 2025Review
- Hypoxic pregnancy promotes fibrosis and increases stress metabolites in the ovine fetal liver.The Journal of physiology · 2025Article
- Application of Proteomics in Maternal and Neonatal Health: Advancements and Future Directions.Proteomics. Clinical applications · 2025Review
- Article
- Increased hepatic glucose production with lower oxidative metabolism in the growth-restricted fetus.JCI insight · 2024Article
- Review
- The Impact of SLC2A8 RNA Interference on Glucose Uptake and the Transcriptome of Human Trophoblast Cells.Cells · 2024Article
- Dysfunctional Postnatal Mitochondrial Energy Metabolism in a Patient with Neurodevelopmental Defects Caused by Intrauterine Growth Restriction Due to Idiopathic Placental Insufficiency.International journal of molecular sciences · 2024Article
- Serine Administration Improves Selenium Status, Oxidative Stress, and Mitochondrial Function in Longissimus Dorsi Muscle of Piglets with Intrauterine Growth Retardation.Biological trace element research · 2023Article
- Blood pressure and kidney function in neonates and young infants with intrauterine growth restriction.Pediatric nephrology (Berlin, Germany) · 2023Article
- Intrauterine growth restriction in piglets modulates postnatal immune function and hepatic transcriptional responses independently of energy intake.Frontiers in physiology · 2023Article
- Maternal Calorie Restriction Induces a Transcriptional Cytoprotective Response in Embryonic Liver Partially Dependent on Nrf2.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Intrauterine growth restriction (IUGR) of the fetus, resulting from placental insufficiency (PI), is characterized by low fetal oxygen and nutrient concentrations that stunt growth rates of metabolic organs. Numerous animal models of IUGR recapitulate pathophysiological conditions found in human fetuses with IUGR. These models provide insight into metabolic dysfunction in skeletal muscle and liver. For example, cellular energy production and metabolic rate are decreased in the skeletal muscle and liver of IUGR fetuses. These metabolic adaptations demonstrate that fundamental processes in mitochondria, such as substrate utilization and oxidative phosphorylation, are tempered in response to low oxygen and nutrient availability. As a central metabolic organelle, mitochondria coordinate cellular metabolism by coupling oxygen consumption to substrate utilization in concert with tissue energy demand and accretion. In IUGR fetuses, reducing mitochondrial metabolic capacity in response to nutrient restriction is advantageous to ensure fetal survival. If permanent, however, these adaptations may predispose IUGR fetuses toward metabolic diseases throughout life. Furthermore, these mitochondrial defects may underscore developmental programming that results in the sequela of metabolic pathologies. In this review, we examine how reduced nutrient availability in IUGR fetuses impacts skeletal muscle and liver substrate catabolism, and discuss how enzymatic processes governing mitochondrial function, such as the tricarboxylic acid cycle and electron transport chain, are regulated. Understanding how deficiencies in oxygen and substrate metabolism in response to placental restriction regulate skeletal muscle and liver metabolism is essential given the importance of these tissues in the development of later lifer metabolic dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.