ArticleCell death discovery2025
Atorvastatin improves spermatogenesis in murine and in vitro human chronic orchitis models through restoring blood-testis barriers.
Article in Cell death discovery, 2025. 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.
- Effects of dietary supplementation with polyphenolic extracts from Lasia spinosa Thw. roots on reproductive performance in Guangxi Ma Roosters.Poultry science · 2026Article
- Quercetin upregulates steroid hormone biosynthesis to enhance reproductive performance in roosters.Poultry science · 2026Article
- Inflammation-Driven Remodeling of the Blood-Testis Barrier: Roles of Junctional Complexes, Actin Dynamics, and Kinase Signaling.Biomedicines · 2026Review
- Atorvastatin Safety Reappraised: From Pharmacogenomic Mechanisms to Personalized Risk Management.Cardiovascular therapeutics · 2026Review
- Advances in immune-inflammatory interactions within the testicular-penile microenvironment of varicocele patients: molecular mechanisms underlying erectile dysfunction and spermatogenic impairment.Frontiers in endocrinology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
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Abstract
Chronic orchitis, which stems from autoimmune responses and infections, significantly impairs the testicular niche and affects male fertility. However, there is a lack of effective therapeutic drugs. In this study, we aimed to explore whether atorvastatin can be used for the treatment of chronic orchitis and the underlying mechanism based on our previous findings and detection using the database. We utilized mouse models of chronic orchitis induced by both autoimmune and infectious causes to demonstrate that atorvastatin can markedly improve spermatogenesis and fertility. Mechanism studies through single-cell transcriptomic analysis, target gene knockdown, quantitative proteomics, and small molecule interference revealed that atorvastatin suppressed the Rac1/AP1/MMPs pathway via inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) in Sertoli cells, thereby restoring the blood-testis barrier (BTB) and spermatogenesis. More importantly, atorvastatin also re-established the expression of BTB-associated proteins and increased the germ cell numbers in cultured human testis tissues. Collectively, our study reveals the essential impact of atorvastatin in improving spermatogenesis in murine and human chronic orchitis models through restoring BTB and suggests that atorvastatin as a promising agent for the clinical treatment of chronic orchitis.
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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.