ArticleScientific reports2017
Testis Transcriptome Modulation in Klinefelter Patients with Hypospermatogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Sex chromosome aneuploidy impacts on human gene expression and regulation: a systematic review.Molecular medicine (Cambridge, Mass.) · 2025Pooled it
- POU4F2/Brn-3b is Essential for Spermatogenesis and its Disruption is Linked to Male Infertility in Mice and Humans.Research square · 2025Article
- The multi-omic landscape of sex chromosome abnormalities: current status and future directions.Endocrine connections · 2023Review
- Review
- New developments and future trajectories in supernumerary sex chromosome abnormalities: a summary of the 2022 3rd International Workshop on Klinefelter Syndrome, Trisomy X, and XYY.Endocrine connections · 2023Review
- Transcriptomic differences between fibrotic and non-fibrotic testicular tissue reveal possible key players in Klinefelter syndrome-related testicular fibrosis.Scientific reports · 2022Article
- Candidate genes for infertility: an in-silico study based on cytogenetic analysis.BMC medical genomics · 2022Article
- Comparative single-cell analysis of biopsies clarifies pathogenic mechanisms in Klinefelter syndrome.American journal of human genetics · 2021Article
- How Successful Is Surgical Sperm Retrieval in Klinefelter Syndrome?Frontiers in reproductive health · 2021Review
- Expression profile of microRNAs in the testes of patients with Klinefelter syndrome.Scientific reports · 2020Article
- Deletion ofFrontiers in genetics · 2020Article
- Resolvin D1 Reduces Lung Infection and Inflammation Activating Resolution in Cystic Fibrosis.Frontiers in immunology · 2020Article
- Modeling Klinefelter Syndrome Using Induced Pluripotent Stem Cells Reveals Impaired Germ Cell Differentiation.Frontiers in cell and developmental biology · 2020Article
- Blood Testis Barrier and Somatic Cells Impairment in a Series of 35 Adult Klinefelter Syndrome Patients.International journal of molecular sciences · 2019Article
- Human induced pluripotent stem cells from two azoospermic patients with Klinefelter syndrome show similar X chromosome inactivation behavior to female pluripotent stem cells.Human reproduction (Oxford, England) · 2019Article
- Paediatric and adult-onset male hypogonadism.Nature reviews. Disease primers · 2019Review
- Transcriptome analysis of the adult human Klinefelter testis and cellularity-matched controls reveals disturbed differentiation of Sertoli- and Leydig cells.Cell death & disease · 2018Article
- Article
- Infertility in Patients With Klinefelter Syndrome: Optimal Timing for Sperm and Testicular Tissue Cryopreservation.Reviews in urology · 2018Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The main genetic cause of male infertility is represented by the Klinefelter Syndrome (KS), a condition accounting for 3% of all cases of infertility and up to15% of cases of azoospermia. KS is generally characterized by azoospermia; approximately 10% of cases have severe oligozoospermia. Among these, the 30-40% of patients show hypospermatogenesis. The mechanisms leading to adult testis dysfunctions are not completely understood. A microarray transcriptome analysis was performed on testis biopsies obtained from three KS patients with hypospermatogenesis and three control subjects. KS testis showed a differential up- and down-regulation of 303 and 747 transcripts, respectively, as compared to controls. The majority of down-regulated transcripts were involved in spermiogenesis failure and testis morphological defects, whereas up-regulated genes were responsible for testis apoptotic processes. Functional analysis of the transcriptionally altered genes indicated a deregulation in cell death, germ cell function and morphology as well as blood-testis-barrier maintenance and Leydig cells activity. These data support a complex scenario in which spermatogenic impairment is the result of functional and morphological alterations in both germinal and somatic components of KS testis. These findings could represent the basis for evaluating new markers of KS spermatogenesis and potential targets of therapeutic intervention to preserve residual spermatogenesis.
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