Evidence map›Paper›PMID 35409285›Full record

SynthesisInternational journal of molecular sciences2022

Sperm Ion Transporters and Channels in Human Asthenozoospermia: Genetic Etiology, Lessons from Animal Models, and Clinical Perspectives.

Emma Cavarocchi, Marjorie Whitfield, Fabrice Saez, Aminata Touré

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  9. Comparison of different processed products ofTranslational andrology and urology · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. SLO3: A Conserved Regulator of Sperm Membrane Potential.International journal of molecular sciences · 2023
    Review
  16. Article
  17. Review
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  19. 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

4 authors at 1 institution in 1 country.

Emma CavarocchiInstitute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, 38000 Grenoble, France.ORCID 0000-0001-9652-1094
Marjorie WhitfieldInstitute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, 38000 Grenoble, France.
Fabrice SaezUMR GReD Institute (Génétique Reproduction & Développement) CNRS 6293, INSERM U1103, Team «Mécanismes de L'Infertilité Mâle Post-Testiculaire», Université Clermont Auvergne, 63000 Clermont-Ferrand, France.ORCID 0000-0001-9570-3777
Aminata TouréInstitute for Advanced Biosciences, INSERM U1209, CNRS UMR5309, Université Grenoble Alpes, 38000 Grenoble, France.ORCID 0000-0001-5629-849X
Centre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche ANR 19-CE17-0014Grenoble Alpes University IRGA-SPERMOBIL 2021
6 · The paper itself

Abstract

In mammals, sperm fertilization potential relies on efficient progression within the female genital tract to reach and fertilize the oocyte. This fundamental property is supported by the flagellum, an evolutionarily conserved organelle that provides the mechanical force for sperm propulsion and motility. Importantly several functional maturation events that occur during the journey of the sperm cells through the genital tracts are necessary for the activation of flagellar beating and the acquisition of fertilization potential. Ion transporters and channels located at the surface of the sperm cells have been demonstrated to be involved in these processes, in particular, through the activation of downstream signaling pathways and the promotion of novel biochemical and electrophysiological properties in the sperm cells. We performed a systematic literature review to describe the currently known genetic alterations in humans that affect sperm ion transporters and channels and result in asthenozoospermia, a pathophysiological condition defined by reduced or absent sperm motility and observed in nearly 80% of infertile men. We also present the physiological relevance and functional mechanisms of additional ion channels identified in the mouse. Finally, considering the state-of-the art, we discuss future perspectives in terms of therapeutics of asthenozoospermia and male contraception.

Indexed as

AsthenozoospermiaAnimalsFemaleHumansIon ChannelsMaleMammalsMiceModels, AnimalSpermatozoaSperm MotilityIon Channelsasthenozoospermiagene mutationhumanion channelmousesperm

Identifiers

PMID35409285
PMCPMC8999829
OpenAlexW4223579129

What Socratic holds

Textmetadata
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 Socratic graph.