Evidence map›Paper›PMID 36109553›Full record

ArticleScientific reports2022

The cost of the circadian desynchrony on the Leydig cell function.

Maja V Pavlovic, Dijana Z Marinkovic, Silvana A Andric, Tatjana S Kostic

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Alterations in Pregnenolone and Testosterone Levels in Male Shift Workers.International journal of environmental research and public health · 2023
    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

4 authors at 1 institution in 1 country.

Maja V Pavlovic *Faculty of Sciences and Mathematics, University of Pristina in Kosovska Mitrovica, 38220, Kosovska Mitrovica, Serbia.
Dijana Z Marinkovic *Laboratory for Chronobiology and Aging, Department of Biology and Ecology, Faculty of Sciences, University of Novi Sad, Dositeja Obradovica Sq 2, 21000, Novi Sad, Serbia.
Silvana A AndricLaboratory for Chronobiology and Aging, Department of Biology and Ecology, Faculty of Sciences, University of Novi Sad, Dositeja Obradovica Sq 2, 21000, Novi Sad, Serbia.
Tatjana S KosticLaboratory for Chronobiology and Aging, Department of Biology and Ecology, Faculty of Sciences, University of Novi Sad, Dositeja Obradovica Sq 2, 21000, Novi Sad, Serbia. tatjana.kostic@dbe.uns.ac.rs.
University of Novi Sad · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased frequency of different lifestyles that disrupts circadian rhythms, together with a trend in the accretion of male idiopathic infertility, imposes the necessity to understand the contribution of circadian rhythms disruption to fertility regulation. In this study, the effects of circadian desynchrony (CD) on the steroidogenic capacity of adult Leydig cells were studied. Adult rats were housed under a disturbing light regime (2 days of constant light, 2 days of continual dark, and 3 days of 12:12 h light:dark schedule) designed to mimic shiftwork in humans. CD was characterized by changed and decreased rhythmic locomotor activity and reduced blood testosterone. In the Leydig cells changed transcription of the clock genes (Bmal1, Clock, Cry1 and Reverba/b increased while Per1/2 reversed phase) was detected. This was followed by reduced transcription of genes (Star, Cyp11a1, and Hsd3b1/2) primarily involved in mitosteroidogenesis. In parallel, mitochondrial membrane potential (Δψi) and ATP production declined losing their characteristic oscillatory pattern. Also, the main markers of mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Cytc), fusion (Mfn2), and mitophagy (Pink1 and Tfeb) were disturbed. Collectively, CD targets mitochondria in Leydig cells by reducing mitosteroidogenesis, mitoenergetics, and disturbing mitochondrial dynamics. These changes contribute to testosterone decline compromising androgen-dependent functions, including reproduction.

Indexed as

ARNTL Transcription FactorsLeydig CellsAdenosine TriphosphateAndrogensAnimalsCholesterol Side-Chain Cleavage EnzymeGene Expression RegulationHumansMaleMultienzyme ComplexesProtein KinasesRatsTestosteroneAdenosine TriphosphateAndrogensARNTL Transcription FactorsCholesterol Side-Chain Cleavage EnzymeMultienzyme ComplexesProtein KinasesTestosterone

Identifiers

PMID36109553
PMCPMC9478133
OpenAlexW4295911447

What OpenQuestion holds

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LicenceCC BY
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.