Evidence map›Paper›PMID 28667781›Full record

ReviewJournal of neuroendocrinology2018

Translocator protein (18 kDa): an update on its function in steroidogenesis.

V Papadopoulos, J Fan, B Zirkin

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neuroendocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

55 citing papers in PubMed, 111 citations in OpenAlex.

  1. The Biochemical journal · 2017
    Trial
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  5. Review
  6. Review
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  8. Article
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  10. Article
  11. Review
  12. Article
  13. The Effects of Neuroactive Steroids on Myelin in Health and Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
    Review
  14. Article
  15. Article
  16. Adrenal Dysfunction in Mitochondrial Diseases.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Review
  19. Review
  20. 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

3 authors at 3 institutions in 2 countries.

V PapadopoulosDepartment of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, USA.ORCID 0000-0002-1183-8568
J FanResearch Institute of the McGill University Health Centre, Department of Medicine, McGill University, Montreal, QC, Canada.
B ZirkinDepartment of Biochemistry and Molecular Biology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
Johns Hopkins University · USMcGill University Health Centre · CAUniversity of Southern California · US

Funding

Aging and Leydig Cell FunctionR37AG021092 · NIA · JOHNS HOPKINS UNIVERSITY · PI ZIRKIN, BARRY R · 2006 to 2015
$4.0M
AGING AND LEYDIG CELL FUNCTIONR01AG021092 · NIA · JOHNS HOPKINS UNIVERSITY · PI ZIRKIN, BARRY R · 2002 to 2019
$3.1M
Hypogonadism in Men: Is It Reversible?R21AG051259 · NIA · JOHNS HOPKINS UNIVERSITY · PI ZIRKIN, BARRY R · 2016 to 2017
$446k
NIA NIH HHS R01 AG021092NIA NIH HHS R21 AG051259NIA NIH HHS R37 AG021092
6 · The paper itself

Abstract

Translocator protein (18 kDa) (TSPO) is a ubiquitous mitochondrial protein. Studies of its responses to drug and endogenous ligands have shown TSPO to be involved either directly or indirectly in numerous biological functions, including mitochondrial cholesterol transport and steroid hormone biosynthesis, porphyrin transport and heme synthesis, apoptosis, cell proliferation, and anion transport. Localised to the outer mitochondrial membrane of steroidogenic cells, TSPO has been shown to associate with cytosolic and mitochondrial proteins as part of a large multiprotein complex involved in mitochondrial cholesterol transport, the rate-limiting step in steroidogenesis. There is general agreement as to the structure and pharmacology of TSPO. Stimulation of TSPO has been shown to have therapeutic use as anxiolytics by inducing allopregnanolone production in the brain, and also potentially for re-establishing androgen levels in hypogonadal ageing animals. Until recently, there has been general agreement regarding the role of TSPO in steroidogenesis. However, recent studies involving genetic depletion of TSPO in mice have created controversy about the role of this protein in steroid and heme synthesis. We review the data on the structure and function of TSPO, as well as the recent results obtained using various genetic animal models. Taken together, these studies suggest that TSPO is a unique mitochondrial pharmacological target for diseases that involve increased mitochondrial activity, including steroidogenesis. Although there is no known mammalian species that lacks TSPO, it is likely that, because of the importance of this ancient protein in evolution and mitochondrial function, redundant mechanisms may exist to replace it under circumstances when it is removed.

Indexed as

AnimalsApoptosisCell ProliferationFemaleGonadal Steroid HormonesMaleMiceMitochondriaReceptors, GABAGonadal Steroid HormonesReceptors, GABAmitochondrianeuroactive steroidssteroidstranslocator protein

Identifiers

PMID28667781
PMCPMC5748373
OpenAlexW2734311660

What OpenQuestion holds

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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.