Evidence map›Paper›PMID 23435356›Full record

ArticleBiochemical pharmacology2013

Tryptophan hydroxylase-2: an emerging therapeutic target for stress disorders.

Guo-Lin Chen, Gregory M Miller

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Effects ofJournal of neurology, neurosurgery, and psychiatry · 2020
    Article
  9. Article
  10. Article
  11. Frontiers in pharmacology · 2018
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
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 1 country.

Guo-Lin ChenHarvard Medical School, New England Primate Research Center, Division of Neuroscience, One Pine Hill Drive, Southborough, MA 01772-9102, USA. guo-lin_chen@hms.harvard.edu
Gregory M Miller
Harvard University · USNew England Biolabs (United States) · US

Funding

New England Primate Research Center Base GrantP51OD011103 · OD · HARVARD MEDICAL SCHOOL · PI FLIER, JEFFREY S · 2012 to 2013
$24.7M
Epigenetic Regulation of Serotonin:Relevance to HIV and Methamphetamine AbuseR21DA030177 · NIDA · HARVARD MEDICAL SCHOOL · PI MILLER, GREGORY MICHAEL · 2010 to 2012
$928k
Drug Abuse-related Neurobiology and Genetic Variance Modeled in Rhesus MonkeysK02DA025697 · NIDA · HARVARD MEDICAL SCHOOL · PI MILLER, GREGORY MICHAEL · 2009 to 2013
$615k
NIDA NIH HHS DA025697NIDA NIH HHS DA030177NIDA NIH HHS K02 DA025697NIDA NIH HHS R21 DA030177NIH HHS P51 OD011103
6 · The paper itself

Abstract

Serotonin (5-HT) has been long recognized to modulate the stress response, and dysfunction of 5-HT has been implicated in numerous stress disorders. Accordingly, the 5-HT system has been targeted for the treatment of stress disorders. Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in 5-HT synthesis, and the recent identification of a second, neuron-specific TPH isoform (TPH2) opened up a new area of research. With a decade of extensive investigation, it is now recognized that: (1) TPH2 exhibits a highly flexible gene expression that is modulated by an increasing number of internal and external environmental factors including the biological clock, stressors, endogenous hormones, and antidepressant therapies; and (2) genetically determined TPH2 activity is linked to a growing body of stress-related neuronal correlates and behavioral traits. These findings reveal an active role of TPH2 in the stress response and provide new insights into the long recognized but not yet fully understood 5-HT-stress interaction. As a major modulator of 5-HT neurotransmission and the stress response, TPH2 is of both pathophysiological and pharmacological significance, and is emerging as a new therapeutic target for the treatment of stress disorders. Given that numerous antidepressant therapies influence TPH2 gene expression, TPH2 is already inadvertently targeted for the treatment of stress disorders. With increased understanding of the regulation of TPH2 activity we can now purposely utilize TPH2 as a target to develop new or optimize current therapies, which are expected to greatly improve the prevention and treatment of a wide variety of stress disorders.

Indexed as

Stress, PhysiologicalAnimalsAnxietyCircadian RhythmDepressionFatigue Syndrome, ChronicGene ExpressionHumansIsoenzymesMolecular Targeted TherapyNeuronsPolymorphism, GeneticSpecies SpecificityStress, PsychologicalTryptophan HydroxylaseIsoenzymesTryptophan Hydroxylase

Identifiers

PMID23435356
PMCPMC3727219
OpenAlexW2013201036

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.