ArticleScientific reports2025
HMG-CoA reductase inhibition preserves testicular function after torsion/detorsion by modulating oxidative stress and AKT signaling.
Article in Scientific reports, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Effects of Iloprost on TRPM7-Mediated Apoptosis and Oxidative Stress in an Experimental Testicular Torsion-Detorsion Model.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Testicular torsion (TT) is a urological emergency that results in ischemia/reperfusion (I/R) injury, leading to oxidative stress, cellular apoptosis, and impaired spermatogenesis. This study investigated the protective effects of the HMG-CoA reductase inhibitor rosuvastatin on TT-induced I/R injury and explored the underlying mechanisms. Male Balb/C mice (n = 28) were subjected to 720° testicular torsion for two hours, followed by 24 h of detorsion. Rosuvastatin was administered either acutely (post-torsion) or prophylactically (prior to injury). Histopathological evaluation, assessment of oxidative stress parameters, sperm motility and morphology analysis, and Western blot examination of survival and stress related signaling proteins (pAKT, pJNK1/2, pERK1/2, and Bcl-xL) were performed. Rosuvastatin treatment significantly reduced tissue damage decreased oxidative stress (as indicated by increased TAS and reduced TOS/OSI), and improved sperm motility and morphology. Both acute and prophylactic treatment regimens enhanced cell survival by increasing pAKT and Bcl-xL levels, reducing pERK1/2 activation, and modulating stress responsive JNK1/2 signaling. These findings suggest that rosuvastatin mitigates I/R induced testicular damage primarily through modulation of key intracellular pathways, particularly PI3K/AKT, and support its therapeutic potential in acute testicular injuries and related degenerative conditions.
Indexed as
Identifiers
What OpenQuestion holds
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.