ArticleCell biology and toxicology2023
Hyperhomocysteinemia lowers serum testosterone concentration via impairing testosterone production in Leydig cells.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Association between serum vitamins and sex hormone levels in adolescent males: based on the National Health and Nutrition Examination Survey (NHANES).Hormones (Athens, Greece) · 2026Article
- Role of Vitamin B₆ in Testosterone Synthesis.The world journal of men's health · 2026Review
- Outcome-specific shifts in homocysteine-androgen correlations in polycystic ovary syndrome.Frontiers in endocrinology · 2026Article
- Seminal Homocysteine Levels in Men With Asthenozoospermia: Correlation With Sperm Parameters and Vitamin BTheScientificWorldJournal · 2026Article
- The mechanistic role of cardiac glycosides in DNA damage response and repair signaling.Cellular and molecular life sciences : CMLS · 2023Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Hyperhomocysteinemia (HHcy) plays a salient role in male infertility. However, whether HHcy interferes with testosterone production remains inconclusive. Here, we reported a lower serum testosterone level in HHcy mice. Single-cell RNA sequencing revealed that genes related to testosterone biosynthesis, together with nuclear receptor subfamily 5 group A member 1 (Nr5a1), a key transcription factor for steroidogenic genes, were downregulated in the Leydig cells (LCs) of HHcy mice. Mechanistically, Hcy lowered trimethylation of histone H3 on lysine 4 (H3K4me3), which was bound on the promoter region of Nr5a1, resulting in downregulation of Nr5a1. Intriguingly, we identified an unknown cell cluster annotated as Macrophage-like Leydig cells (McLCs), expressing both LCs and macrophages markers. In HHcy mice, McLCs were shifted toward pro-inflammatory phenotype and thus promoted inflammatory response in LC. Betaine supplementation rescued the downregulation of NR5A1 and restored the serum testosterone level in HHcy mice. Overall, our study highlights an etiological role of HHcy in LCs dysfunction.
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Registered trials
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