ArticleBiology of reproduction2014
Loss of smad4 in Sertoli and Leydig cells leads to testicular dysgenesis and hemorrhagic tumor formation in mice.
Article in Biology of reproduction, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Bta-miR-146a Inhibits Proliferation and Promotes Apoptosis of Bovine Immature Sertoli Cells by Targeting SMAD4 via the TGF-β/MAPK Signaling Pathway.International journal of molecular sciences · 2026Article
- Comparison of reproductive performance and functional analysis of spermatogenesis factors between domestic yak and semi-wild blood yak.BMC genomics · 2025Article
- Sertoli cells as a hub in testicular development and male reproductive.Frontiers in cell and developmental biology · 2025Review
- Functional Study of PTSMAD4 in the Spermatogenesis of the Swimming CrabInternational journal of molecular sciences · 2024Article
- Transcriptomic Study of Different Stages of Development in the Testis of Sheep.Animals : an open access journal from MDPI · 2024Article
- SMAD4 mutations causing Myhre syndrome are under positive selection in the male germline.American journal of human genetics · 2024Article
- Oral vaccination with inhibin DNA vaccine for promoting spermatogenesis in rats.Animal reproduction · 2024Article
- Hyperhomocysteinemia lowers serum testosterone concentration via impairing testosterone production in Leydig cells.Cell biology and toxicology · 2023Article
- Association between sperm mitochondarial DNA copy number and nuclear DNA methylation.Epigenomics · 2020Article
- Article
- Multiple signaling pathways in Sertoli cells: recent findings in spermatogenesis.Cell death & disease · 2019Review
- Genetic intersection of male infertility and cancer.Fertility and sterility · 2018Review
- Expression, Localization of SUMO-1, and Analyses of Potential SUMOylated Proteins inFrontiers in physiology · 2017Article
- Novel Targets for the Transcription Factors MEF2 in MA-10 Leydig Cells.Biology of reproduction · 2015Article
- The Warburg effect revisited--lesson from the Sertoli cell.Medicinal research reviews · 2015Review
- Bone Morphogenetic Protein (BMP) signaling in development and human diseases.Genes & diseases · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
As the central component of canonical TGFbeta superfamily signaling, SMAD4 is a critical regulator of organ development, patterning, tumorigenesis, and many other biological processes. Because numerous TGFbeta superfamily ligands are expressed in developing testes, there may exist specific requirements for SMAD4 in individual testicular cell types. Previously, we reported that expansion of the fetal testis cords requires expression of SMAD4 by the Sertoli cell lineage. To further uncover the role of Smad4 in murine testes, we produced conditional knockout mice lacking Smad4 in either Leydig cells or in both Sertoli and Leydig cells simultaneously. Loss of Smad4 concomitantly in Sertoli and Leydig cells led to underdevelopment of the testis cords during fetal life and mild testicular dysgenesis in young adulthood (decreased testis size, partially dysgenic seminiferous tubules, and low sperm production). When the Sertoli/Leydig cell Smad4 conditional knockout mice aged (56- to 62-wk old), the testis phenotypes became exacerbated with the appearance of hemorrhagic tumors, Leydig cell adenomas, and a complete loss of spermatogenesis. In contrast, loss of Smad4 in Leydig cells alone did not appreciably alter fetal and adult testis development. Our findings support a cell type-specific requirement of Smad4 in testis development and suppression of testicular tumors.
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Registered trials
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.