ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Sertoli Cell-Derived Extracellular Vesicles Orchestrate Cadmium-Induced Testicular Inflammation and Fibrosis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
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Who cites it
1 citing paper in PubMed.
- Platelet-Derived Growth Factor Receptor Alpha in Male Reproductive Health and Oxidative Stress: Stromal Homeostasis, Injury, and Research Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
Cadmium (Cd) is a widespread environmental toxicant that impairs male reproductive health, though its testicular toxicity mechanisms remain incompletely defined. Combining single-cell RNA sequencing with functional assays, we identified a novel intercellular communication pathway mediated by Sertoli cell-derived extracellular vesicles (EVs) in Cd-induced testicular injury. In mice, Cd exposure caused testicular atrophy, spermatogenesis disruption, and fibrosis. Multi-omics analyses revealed activation of multiple programmed cell death pathways, including apoptosis, necroptosis, pyroptosis, and ferroptosis. Single-cell RNA sequencing (scRNA-seq) demonstrated testicular cellular remodeling featuring Sertoli cell depletion and fibroblast expansion. Mechanistically, Cd triggered multi-modal programmed cell death (PCD) in Sertoli cells, promoting EV release enriched with damage-associated molecular patterns (DAMPs) and mitochondrial components. These EVs were internalized by testicular macrophages, activating the TLR4/NF-κB pathway and inducing a pro-inflammatory phenotype. Consequently, activated macrophages stimulated fibroblast-mediated fibrosis via TGF-β/Smad signaling. These findings elucidate a Sertoli cell-EV-macrophage-fibroblast axis in Cd-induced testicular damage, offering new insights into environmental toxicant-induced male infertility and potential therapeutic targets.
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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.