Evidence map›Paper›PMID 29018353›Full record

ArticleFrontiers in physiology2017

Heat Stress Reduces Sperm Motility via Activation of Glycogen Synthase Kinase-3α and Inhibition of Mitochondrial Protein Import.

Yabin Gong, Huiduo Guo, Zhilong Zhang, Hao Zhou, Ruqian Zhao, Bin He

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

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  18. Frontiers in cell and developmental biology · 2024
    Article
  19. Article
  20. The Role of Melatonin to Ameliorate Oxidative Stress in Sperm Cells.International journal of molecular sciences · 2023
    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

6 authors at 1 institution in 1 country.

Yabin GongKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Huiduo GuoKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Zhilong ZhangKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Hao ZhouKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Ruqian ZhaoKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Bin HeKey Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture, Nanjing Agricultural UniversityNanjing, China.
Nanjing Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adverse effects of high environmental temperature exposure on animal reproductive functions have been concerned for many decades. However, the molecular basis of heat stress (HS)-induced decrease of sperm motility has not been entirely elucidated. We hypothesized that the deteriorate effects of HS may be mediated by damage of mitochondrial function and ATP synthesis. To test this hypothesis, we use mature boar sperm as model to explore the impacts of HS on mitochondrial function and sperm motility. A 6 h exposure to 42°C (HS) induced significant decrease in sperm progressive motility. Concurrently, HS induced mitochondrial dysfunction that is indicated by decreased of membrane potential, respiratory chain complex I and IV activities and adenosine triphosphate (ATP) contents. Exogenous ATP abolished this effect suggesting that reduced of ATP synthesis is the committed step in HS-induced reduction of sperm motility. At the molecular level, the mitochondrial protein contents were significantly decreased in HS sperm. Notably, the cytochrome c oxidase subunit 4, which was synthesized in cytoplasm and translocated into mitochondria, was significantly lower in mitochondria of HS sperm. Glycogen synthase kinase-3α (GSK3α), a negative regulator of sperm motility that is inactivated by Ser21 phosphorylation, was dephosphorylated after HS. The GSK3α inhibitor CHIR99021 was able to abolish the effects of HS on sperm and their mitochondria. Taken together, our results demonstrate that HS affects sperm motility through downregulation of mitochondrial activity and ATP synthesis yield, which involves dephosphorylation of GSK3α and interference of mitochondrial remodeling.

Indexed as

glycogen synthase kinase-3αheat stressmitochondrial remodelingoxidative phosphorylationsperm

Identifiers

PMID29018353
PMCPMC5615227
OpenAlexW2756815027

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.