ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019
A young testicular microenvironment protects Leydig cells against age-related dysfunction in a mouse model of premature aging.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- WFS1 Deficiency Impairs PIAS4-Associated SUMOylation and Increases Ubiquitin-Mediated Spermatogenesis-Related Protein Degradation Leading to Testicular Male Infertility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Grtp1 Safeguards Against Paternal Reproductive Aging and Intergenerational Behavioral Deficits by Preserving Redox Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The effects of testicular aging on Leydig cells and the application of stem cells in restoring Leydig cells function.Reproductive biology and endocrinology : RB&E · 2025Review
- Evaluation and research progress on rodent models of late-onset hypogonadism: a comprehensive review.The Canadian journal of urology · 2025Review
- Effects of Aging on Mammalian Spermatogenesis From a Cellular Perspective.Molecular reproduction and development · 2025Review
- Perspectives on biomarkers of reproductive aging for fertility and beyond.Nature aging · 2024Review
- Age-related testosterone decline: mechanisms and intervention strategies.Reproductive biology and endocrinology : RB&E · 2024Review
- Delivery of low-density lipoprotein from endocytic carriers to mitochondria supports steroidogenesis.Nature cell biology · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Article
- Testicular aging, male fertility and beyond.Frontiers in endocrinology · 2022Review
- Emerging concepts on Leydig cell development in fetal and adult testis.Frontiers in endocrinology · 2022Review
- Expression of the NSE,SP,NFH and DβH in normal and cryptorchid testes of Bactrian camel.Animal reproduction · 2022Article
- Review
- Advances in stem cell research for the treatment of primary hypogonadism.Nature reviews. Urology · 2021Review
- Ablation of the canonical testosterone production pathway via knockout of the steroidogenic enzyme HSD17B3, reveals a novel mechanism of testicular testosterone production.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Restorative functions of Autologous Stem Leydig Cell transplantation in a Testosterone-deficient non-human primate model.Theranostics · 2020Article
- Human Adipose-derived Pericytes Display Steroidogenic Lineage Potential in Vitro and Influence Leydig Cell Regeneration in Vivo in Rats.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 7 institutions in 3 countries.
Funding
Abstract
Testicular Leydig cells (LCs) are the primary source of circulating androgen in men. As men age, circulating androgen levels decline. However, whether reduced LC steroidogenesis results from specific effects of aging within LCs or reflects degenerative alterations to the wider supporting microenvironment is unclear; inability to separate intrinsic LC aging from that of the testicular microenvironment in vivo has made this question difficult to address. To resolve this, we generated novel mouse models of premature aging, driven by CDGSH iron sulfur domain 2 ( Cisd2) deletion, to separate the effects of cell intrinsic aging from extrinsic effects of aging on LC function. At 6 mo of age, constitutive Cisd2-deficient mice display signs of premature aging, including testicular atrophy, reduced LC and Sertoli cell (SC) number, decreased circulating testosterone, increased luteinizing hormone/testosterone ratio, and decreased expression of steroidogenic mRNAs, appropriately modeling primary testicular dysfunction observed in aging men. However, mice with Cisd2 deletion (and thus premature aging) restricted to either LCs or SCs were protected against testicular degeneration, demonstrating that age-related LCs dysfunction cannot be explained by intrinsic aging within either the LC or SC lineages alone. We conclude that age-related LC dysfunction is largely driven by aging of the supporting testicular microenvironment.-Curley, M., Milne, L., Smith, S., Jørgensen, A., Frederiksen, H., Hadoke, P., Potter, P., Smith, L. B. A Young testicular microenvironment protects Leydig cells against age-related dysfunction in a mouse model of premature aging.
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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.