ArticleReproductive sciences (Thousand Oaks, Calif.)2012
Mid-gestation ovine cardiomyocytes are vulnerable to mitotic suppression by thyroid hormone.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 28 citations in OpenAlex.
- Fetal cardiac troponin I levels decline toward birth in sheep.American journal of physiology. Heart and circulatory physiology · 2024Article
- Thyroid hormone increases fatty acid use in fetal ovine cardiac myocytes.Physiological reports · 2023Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Developmental changes of the fetal and neonatal thyroid gland and functional consequences on the cardiovascular system.Journal of perinatology : official journal of the California Perinatal Association · 2022Review
- Harnessing conserved signaling and metabolic pathways to enhance the maturation of functional engineered tissues.NPJ Regenerative medicine · 2022Review
- Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.Biology · 2022Review
- Thyroid hormone-dependent regulation of metabolism and heart regeneration.The Journal of endocrinology · 2022Review
- The role of hormones and neurons in cardiomyocyte maturation.Seminars in cell & developmental biology · 2021Review
- Hyperthyroidism in pregnancy: evidence and hypothesis in fetal programming and development.Endocrine connections · 2021Review
- Changes in Cardiomyocyte Cell Cycle and Hypertrophic Growth During Fetal to Adult in Mammals.Journal of the American Heart Association · 2021Review
- Postnatal Growth Restriction in Mice Alters Cardiac Protein Composition and Leads to Functional Impairment in Adulthood.International journal of molecular sciences · 2020Article
- Thyroid Hormone Signalling: From the Dawn of Life to the Bedside.Journal of molecular evolution · 2020Review
- Postnatal Cardiac Development and Regenerative Potential in Large Mammals.Pediatric cardiology · 2019Review
- Thyroid hormone signaling and consequences for cardiac development.The Journal of endocrinology · 2019Review
- Thyroid hormone receptor function in maturing ovine cardiomyocytes.The Journal of physiology · 2019Article
- Cardiac myocyte proliferation and maturation near term is inhibited by early gestation maternal testosterone exposure.American journal of physiology. Heart and circulatory physiology · 2018Article
- Glucocorticoids, antenatal corticosteroid therapy and fetal heart maturation.Journal of molecular endocrinology · 2018Review
- Near to One's Heart: The Intimate Relationship Between the Placenta and Fetal Heart.Frontiers in physiology · 2018Review
- Endocrine and other physiologic modulators of perinatal cardiomyocyte endowment.The Journal of endocrinology · 2016Review
- Thyroid hormone does not induce maturation of embryonic chicken cardiomyocytes in vitro.Physiological reports · 2014Article
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 1 country.
Funding
Abstract
Circulating fetal 3,3',5-tri-iodo-l-thyronine (T(3) ) is maintained at very low levels until a dramatic prepartum surge. 3,3',5-Tri-iodo-l-thyronine inhibits serum-stimulated proliferation in near-term ovine cardiomyocytes, but it is not known whether midgestation myocytes are also inhibited. Because early cessation of cardiomyocyte mitosis would result in an underendowed heart, we hypothesized that 0.67 gestation (100 of 145 days gestation) ovine cardiomyocytes would be insensitive to suppressive growth effects of T(3) . These younger cardiomyocytes were grown with T(3) in 10% serum-enriched media for 24 hours. Physiological (0.37, 0.75, and 1.5 nmol/L) concentrations of T(3) dramatically suppressed mitotic activity in cardiomyocytes (P < .001). 3,3',5-Tri-iodo-l-thyronine stimulated phosphorylation of extracellular signal-regulated kinase and AKT (also known as Protein Kinase B [PKB]) signaling pathways. Nevertheless, the protein content of the cell cycle suppressor, p21, increased 2-fold (P < .05), and promoter, cyclin D1, decreased by 50%. Contrary to our hypothesis, elevated levels of T(3) powerfully inhibit proliferation of midgestation fetal cardiomyocytes. Thus, midgestation maternal hyperthyroidism might lead to an underendowed fetal myocardium.
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.