Evidence map›Paper›PMID 31117055›Full record

ReviewThe Journal of endocrinology2019

Thyroid hormone signaling and consequences for cardiac development.

Natasha N Chattergoon

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
13.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. A genome-wide interaction study of thyroid-stimulating hormone levels and particulate matter exposure among Koreans.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Overlapping action of TFrontiers in endocrinology · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Purinergic signaling in thyroid disease.Purinergic signalling · 2023
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Natasha N ChattergoonCenter for Developmental Health, Oregon Health and Science University, Portland, Oregon, USA.
Oregon Health & Science University · US

Funding

ULTRASOUND IMAGING COREP01HD034430 · NICHD · OREGON HEALTH & SCIENCE UNIVERSITY · PI GIRAUD, GEORGE D · 1997 to 2017
$20.7M
Thyroid regulation of cardiomyocyte maturationR01HL102763 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI THORNBURG, KENT L.R. · 2010 to 2013
$1.5M
The unique role of B-Raf in murine cardiac development and postnatal functionK01HL118677 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI CHATTERGOON, NATASHA N · 2013 to 2017
$705k
NHLBI NIH HHS K01 HL118677NHLBI NIH HHS R01 HL102763NICHD NIH HHS P01 HD034430
6 · The paper itself

Abstract

The fetal heart undergoes its own growth and maturation stages all while supplying blood and nutrients to the growing fetus and its organs. Immature contractile cardiomyocytes proliferate to rapidly increase and establish cardiomyocyte endowment in the perinatal period. Maturational changes in cellular maturation, size and biochemical capabilities occur, and require, a changing hormonal environment as the fetus prepares itself for the transition to extrauterine life. Thyroid hormone has long been known to be important for neuronal development, but also for fetal size and survival. Fetal circulating 3,5,3'-triiodothyronine (T3) levels surge near term in mammals and are responsible for maturation of several organ systems, including the heart. Growth factors like insulin-like growth factor-1 stimulate proliferation of fetal cardiomyocytes, while thyroid hormone has been shown to inhibit proliferation and drive maturation of the cells. Several cell signaling pathways appear to be involved in this complicated and coordinated process. The aim of this review was to discuss the foundational studies of thyroid hormone physiology and the mechanisms responsible for its actions as we speculate on potential fetal programming effects for cardiovascular health.

Indexed as

Signal TransductionAnimalsCardiovascular DiseasesCell ProliferationFemaleFetal DevelopmentFetal HeartHeartHeart DiseasesHumansModels, AnimalMyocytes, CardiacPancreasPregnancyPregnancy, AnimalPrenatal Exposure Delayed EffectsThyroid HormonesTriiodothyroninecardiomyocyte maturationfetal programmingoutcomesthyroid hormone

Identifiers

PMID31117055
PMCPMC6613780
OpenAlexW2946201433

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.