ArticleMolecular therapy. Nucleic acids2024
The role of Sertoli cell-derived miR-143-3p in male fertility declines with age.
Article in Molecular therapy. Nucleic acids, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Testicular ageing as a central hallmark of male senescence: characteristics, molecular mechanisms and emerging therapeutic strategies.Annals of medicine · 2026Review
- Clove-Chitosan Nanoparticles Alleviate Fertility Impairment and Reproductive Dysfunction in Obese Male Rat Model.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Analysis of the characteristics of microRNA expression profiles and reproductive regulation-mediated signalling pathways in testicular sertoli derived sEVs from Leizhou goats.Veterinary research communications · 2026Article
- Gene regulation by non-Coding RNAs in infertility: a mechanistic review.Journal of ovarian research · 2025Review
- Extracellular vesicles in dairy cattle: research progress and prospects for practical applications.Journal of animal science and biotechnology · 2025Review
- Seminal Plasma Extracellular Vesicles: Key Mediators of Intercellular Communication in Mammalian Reproductive Systems.Veterinary sciences · 2025Review
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Authors and funding
16 authors.
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Abstract
As delayed parenthood becomes more prevalent, understanding age-related testosterone decline and its impact on male fertility has gained importance. However, molecular mechanisms concerning testicular aging remain largely undiscovered. Our study highlights that miR-143-3p, present in aging Sertoli cells (SCs), is loaded into extracellular vesicles (EVs), affecting Leydig cells (LCs) and germ cells, thus disrupting testicular tissue homeostasis and spermatogenesis. Intriguingly, in SCs, transforming growth factor-β signaling promotes miR-143 precursors transcription, increasing mature miR-143-3p levels. This inhibits Smurf2, activating Smad2, and further enhancing miR-143-3p accumulation. EVs transporting miR-143-3p, originating from SCs, contribute to the age-related decline of testosterone and male fertility by targeting the luteinizing hormone receptor and retinoic acid receptor. Diminishing endogenous miR-143-3p in SCs postpones testis aging, preserving and prolonging male fertility. Thus, our study identified miR-143-3p as a key regulator of testicular function and fertility, revealing miR-143-3p as a potential therapeutic target for male abnormal sexual and reproductive function.
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