ArticleSexual medicine2023
Low androgen levels induce ferroptosis of rat penile cavernous endothelial cells.
Article in Sexual medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Research progress of ferroptosis in obesity and its complications.Journal of physiology and biochemistry · 2026Review
- Seasonal Patterns in Erectile Dysfunction Severity.Cureus · 2025Article
- Icariin inhibits hyperglycemia-induced cell death in penile cavernous tissue and improves erectile function in type 1 diabetic rats.Sexual medicine · 2025Article
- Ferroptosis in thyroid cancer: mechanisms, current status, and treatment.Frontiers in oncology · 2025Review
- Metabolic Syndrome-Associated Erectile Dysfunction: Multiple Vascular Endothelial Dysfunction Mechanisms and Potential Therapeutic Targets.International journal of biological sciences · 2025Review
- Liver iron stores and effectors of ferroptosis are dependent on age and sex.Experimental physiology · 2024Article
- A low androgenic state inhibits erectile function by suppressing endothelial glycosides in the penile cavernous tissue of rats.Sexual medicine · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Endothelial dysfunction caused by low androgen levels in penile tissue can lead to erectile dysfunction. The exact mechanism of endothelial dysfunction has not been thoroughly studied. Objective: The study sought to verify whether low androgen levels induce ferroptosis of endothelial cells in rat penile tissue. Methods: Rat penile cavernous endothelial cells (CP-R133) were divided into a no-androgen group (Dihydrotestosterone (DHT): 0 nmol/L), very low-androgen group (DHT: 0.1 nmol/L), low-androgen group (DHT: 1 nmol/L), DHT = 10 nmol/L group, DHT (0 nmol/L) + ferrostatin-1 (Fer-1) group, DHT (0.1 nmol/L) + Fer-1 group, DHT (1 nmol/L) + Fer-1 group, DHT (10 nmol/L) + Fer-1 group. Cell viability, intracellular ferrous ion (Fe Outcomes: Low androgen levels could induce ferroptosis of rat penile cavernous endothelial cells in vivo by upregulating the expressions of TfR1 and ACSL4 and downregulating the expressions of SLC7A11 and GPX4. Results: Cell viability, the levels of glutathione (GSH), NO, SLC7A11, GPX4, and p-eNOS/eNOS in the DHT = 0 nmol/L group were lower than those in the other groups ( Clinical Implications: A ferroptosis inhibitor might be a novel drug for treating erectile dysfunction caused by low androgen level. Strengths and Limitations: The results of this study need to be further confirmed in in vitro and in human studies. Meanwhile, further investigation is needed to clarify whether low androgen levels affect ferroptosis of rat penile cavernous smooth muscle and nerve cells. Conclusion: Low androgen levels can induce ferroptosis of endothelial cells in rat penile tissue. Inhibition of ferroptosis can reverse endothelial dysfunction caused by low androgen levels.
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