Evidence map›Paper›PMID 24423980›Full record

ReviewEndocrine reviews2014

Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions.

Csaba Fekete, Ronald M Lechan

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 316 citations in OpenAlex.

  1. Pooled it
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  5. Tanycytes: bloodhounds of the metabolic brain.Trends in endocrinology and metabolism: TEM · 2026
    Review
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85 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Csaba FeketeDepartment of Endocrine Neurobiology (C.F.), Institute of Experimental Medicine, Hungarian Academy of Sciences, 1083 Budapest, Hungary; Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism (C.F., R.M.L.), Tupper Research Institute, Tufts Medical Center, Boston, Massachusetts 02111; and Department of Neuroscience (R.M.L.), Tufts University School of Medicine, Boston, Massachusetts 02111.
Ronald M Lechan
Hungarian Academy of Sciences · HUTufts University · US

Funding

TRH REGULATION/BIOSYNTHESIS IN PARAVENTRICULAR NUCLEUSR01DK037021 · NIDDK · TUFTS MEDICAL CENTER · PI LECHAN, RONALD MICHAEL · 1986 to 2010
$3.9M
TRH REGULATION/BIOSYNTHESIS AND PARAVENTRICULAR NUCLEUSR56DK037021 · NIDDK · TUFTS MEDICAL CENTER · PI LECHAN, RONALD MICHAEL · 2007 to 2007
$201k
NIDDK NIH HHS DK-37021NIDDK NIH HHS R01 DK037021NIDDK NIH HHS R56 DK037021
6 · The paper itself

Abstract

TRH is a tripeptide amide that functions as a neurotransmitter but also serves as a neurohormone that has a critical role in the central regulation of the hypothalamic-pituitary-thyroid axis. Hypophysiotropic TRH neurons involved in this neuroendocrine process are located in the hypothalamic paraventricular nucleus and secrete TRH into the pericapillary space of the external zone of the median eminence for conveyance to anterior pituitary thyrotrophs. Under basal conditions, the activity of hypophysiotropic TRH neurons is regulated by the negative feedback effects of thyroid hormone to ensure stable, circulating, thyroid hormone concentrations, a mechanism that involves complex interactions between hypophysiotropic TRH neurons and the vascular system, cerebrospinal fluid, and specialized glial cells called tanycytes. Hypophysiotropic TRH neurons also integrate other humoral and neuronal inputs that can alter the setpoint for negative feedback regulation by thyroid hormone. This mechanism facilitates adaptation of the organism to changing environmental conditions, including the shortage of food and a cold environment. The thyroid axis is also affected by other adverse conditions such as infection, but the central mechanisms mediating suppression of hypophysiotropic TRH may be pathophysiological. In this review, we discuss current knowledge about the mechanisms that contribute to the regulation of hypophysiotropic TRH neurons under physiological and pathophysiological conditions.

Indexed as

Adaptation, PhysiologicalHumansHypothalamusPituitary GlandThyroid GlandThyrotropin-Releasing HormoneThyrotropin-Releasing Hormone

Identifiers

PMID24423980
PMCPMC3963261
OpenAlexW2033553696

What OpenQuestion holds

Textmetadata
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.