ArticleThe Journal of urology2013
Inhibition of Rho-kinase improves erectile function, increases nitric oxide signaling and decreases penile apoptosis in a rat model of cavernous nerve injury.
Article in The Journal of urology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 65 citations in OpenAlex.
- Serum proteomic signatures and an immune-calcium signaling cascade associated with antipsychotic-related erectile dysfunction in schizophrenia.Scientific reports · 2026Article
- 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
- Advances in erectile dysfunction treatment research: a narrative review.Translational andrology and urology · 2025Review
- Erectile Dysfunction: Treatments, Advances and New Therapeutic Strategies.Brain sciences · 2023Review
- Review
- Molecular pathogenesis and treatment of cavernous nerve injury-induced erectile dysfunction: A narrative review.Frontiers in physiology · 2022Review
- Combination Therapy with a JNK Inhibitor and Hepatocyte Growth Factor for Restoration of Erectile Function in a Rat Model of Cavernosal Nerve Injury: Comparison with a JNK Inhibitor Alone or Hepatocyte Growth Factor Alone.International journal of molecular sciences · 2021Article
- Enhancement of the RhoA/Rho kinase pathway is associated with stress-related erectile dysfunction in a restraint water immersion stress model.Physiological reports · 2021Article
- Restoration of Cavernous Veno-Occlusive Function through Chronic Administration of a Jun-Amino Terminal Kinase Inhibitor and a LIM-Kinase 2 Inhibitor by Suppressing Cavernous Apoptosis and Fibrosis in a Rat Model of Cavernous Nerve Injury: A Comparison with a Phosphodiesterase Type 5 Inhibitor.The world journal of men's health · 2021Article
- Cavernous smooth muscles: innovative potential therapies are promising for an unrevealed clinical diagnosis.International urology and nephrology · 2020Review
- Adipose-derived stem cells modified byNeural regeneration research · 2020Article
- Effect of HongJing I in Treating Erectile Function and Regulating RhoA Pathway in a Rat Model of Bilateral Cavernous Nerve Injury.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Article
- Erectile dysfunction among patients with chronic brucellosis.International journal of impotence research · 2018Article
- S-nitrosylation of NOS pathway mediators in the penis contributes to cavernous nerve injury-induced erectile dysfunction.International journal of impotence research · 2018Article
- Neuroprotective and Nerve Regenerative Approaches for Treatment of Erectile Dysfunction after Cavernous Nerve Injury.International journal of molecular sciences · 2017Review
- RhoA/ROCK activation in major pelvic ganglion mediates caspase-3 dependent nitrergic neuronal apoptosis following cavernous nerve injury.Neural regeneration research · 2017Article
- Association of nNOS and Rho-kinase with age-associated erectile dysfunction in Sprague-Dawley rats.Experimental and therapeutic medicine · 2017Article
- M1 Macrophages Are Predominantly Recruited to the Major Pelvic Ganglion of the Rat Following Cavernous Nerve Injury.The journal of sexual medicine · 2017Article
- Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 5 countries.
Funding
Abstract
purposeBilateral cavernous nerve injury results in up-regulation of ROCK signaling in the penis. This is linked to erectile dysfunction in an animal model of post-prostatectomy erectile dysfunction. We evaluated whether daily treatment with the ROCK inhibitor Y-27632 (Tocris Bioscience, Ellisville, Missouri) would prevent erectile dysfunction in a rat model of bilateral cavernous nerve injury. MATERIALS AND
methodsSprague-Dawley® rats underwent surgery to create sham (14) or bilateral (27) cavernous nerve injury. In the injury group 13 rats received treatment with Y-27632 (5 mg/kg twice daily) and 14 received vehicle. At 14 days after injury, rats underwent cavernous nerve stimulation to determine erectile function. Penes were assessed for neuronal and nitric oxide synthase membrane-endothelial nitric oxide synthase. ROCK2 was assessed by Western blot. Cyclic guanosine monophosphate was determined by enzyme-linked immunosorbent assay. Cavernous homogenates were tested for ROCK and protein kinase G enzymatic activity. Penile apoptosis was evaluated using the Apostain technique (Alexis, San Diego, California). Data were analyzed on ROCK using ANOVA and the t test.
resultsWhile erectile function was decreased in rats with bilateral cavernous nerve injury, daily administration of Y-27632 improved erectile responses. Injury decreased neuronal and nitric oxide synthase membrane-endothelial nitric oxide synthase but ROCK2 was significantly increased. Y-27632 treatment restored neuronal nitric oxide synthase, nitric oxide synthase membrane-endothelial nitric oxide synthase and cyclic guanosine monophosphate levels, and protein kinase G activity. Treatment significantly decreased ROCK2 protein and ROCK activity. There were significantly fewer apoptotic cells after treatment than in injured controls.
conclusionsThese results provide evidence for up-regulation of the RhoA/ROCK signaling pathway with detrimental effects on erectile function after bilateral cavernous nerve injury. ROCK inhibition improved erectile dysfunction associated with bilateral cavernous nerve injury by preserving penile nitric oxide bioavailability and decreasing penile apoptosis.
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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.