Cavernous Nerve Injury by Radiation Therapy May Potentiate Erectile Dysfunction in Rats

Mahmood, Javed; Connors, Caroline Q.; Alexander, A.; Pavlović, Radmila; Samanta, Sukhen; Soman, S.; Matsui, Hotaka; Sopko, Nikolai A.; Bivalacqua, Trinity J.; Weinreich, Daniel; Ho, Cheng Ying; Eley, John G.; Sawant, Amit; Jackson, Isabel L.; Vujašković, Željko

doi:10.1016/j.ijrobp.2017.06.2449

Cited by 23 publications

(12 citation statements)

References 29 publications

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“…Meanwhile, our previous studies investigated the molecular pathway involved in cavernosal fibrosis after CN injuries, and suggested that the ROCK1/LIMK2/Cofilin pathway could contribute to cavernosal fibrosis with loss of SM after CN injuries [17, 18, 23]. In accordance with these, a few recent studies have demonstrated that activated RhoA/ROCK1 or ROCK2 pathway contributes to the development of ED and structural alterations such as cavernosal apoptosis or fibrosis in a rat model of CN injury [19, 20, 29]. According to the study by Gratzke et al, an increased protein expression of RhoA and ROCK2 was observed together with a decrease in erectile response to electrostimulation in a rat model of CNCI [19].…”

Section: Discussionmentioning

confidence: 92%

“…Hannan et al demonstrated that intracavernous injection of ROCK inhibitors improved ED and cavernosal apoptosis through decreased protein expression of ROCK2 and reduced ROCK activity [20]. Interestingly, Mahmood et al showed that radiation-induced CN injury caused ED through an increase of cavernosal fibrosis and apoptosis in rats [29]. Activated RhoA/ROCK1 pathway was involved in the cavernosal fibrosis and apoptosis after radiation-induced CN injury [29].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, Mahmood et al showed that radiation-induced CN injury caused ED through an increase of cavernosal fibrosis and apoptosis in rats [29]. Activated RhoA/ROCK1 pathway was involved in the cavernosal fibrosis and apoptosis after radiation-induced CN injury [29].…”

Section: Discussionmentioning

confidence: 99%

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Chronic administration of LIMK2 inhibitors alleviates cavernosal veno-occlusive dysfunction through suppression of cavernosal fibrosis in a rat model of erectile dysfunction after cavernosal nerve injury

et al. 2019

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We evaluated whether chronic administration of LIMK2-inhibitors could improve erectile function by alleviating CVOD through suppressing cavernosal fibrosis in a rat model of cavernosal nerve crush-injury (CNCI). Forty-two 12-week-old rats were equally categorized into the three groups: sham-surgery (S), CNCI (I), and CNCI treated with LIMK2-inhibitors (L). The L-group was treated with daily intraperitoneal injection of LIMK2-inhibitors (10.0 mg/kg) for 30-days after surgery. Erectile function was assessed using dynamic-infusion-cavernosometry (DIC). Penile tissue was processed for Masson’s-trichrome staining, Western-blotting, and double immunofluorescence. The I-group showed significantly higher maintenance and drop rates as well as lower papaverine response, compared to the S-group. Chronic inhibition of LIMK2 in the L-group significantly improved the DIC parameters compared to those in the I-group, although the parameters were not completely restored to normal control values. Also, the I-group showed a reduced smooth muscle (SM)-to-collagen ratio, decreased immunohistochemical staining for α-SM-actin, increased number of fibroblasts positive for phosphorylated Cofilin, increased LIMK2/Cofilin phosphorylation and increased protein expression of Collagen-1 or Fibronectin, compared to the S-group. The L-group showed significant improvements in SM/collagen ratio and the deposition of Collagen-1 or Fibronectin compared to the I-group, although not completely normalized. According to the densitometry and confocal microscopy results, the L-group showed restoration of LIMK2/Cofilin phosphorylation and amount of fibroblasts positive for phosphorylated Cofilin to the normal control value. In conclusion, chronic inhibition of LIMK2 can improve CVOD and ED by alleviating cavernosal fibrosis via normalizing the LIMK2/Cofilin pathway.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Chronic administration of LIMK2 inhibitors alleviates cavernosal veno-occlusive dysfunction through suppression of cavernosal fibrosis in a rat model of erectile dysfunction after cavernosal nerve injury

et al. 2019

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“…Особенности Экспериментальные исследования на животных (крысы и собаки) в большей степени, чем клинические, указывают на ключевую роль повреждения нервных путей в развитии РИЭД [32,[52][53][54]. Применение количественной полимеразно-цепной реакции, а также иммуногистохимии и трансмиссионной электронной микроскопии позволяют выявить ультраструктурные нарушения в ткани кавернозных нервов, развивающиеся в различные периоды после окончания лучевого воздействия.…”

Section: механизмы развития радиационноиндуцированной эректильной дисunclassified

Radiation-Induced Erectile Dysfunction in Prostate Cancer Patients: Up-to-Date View on Pathogenesis

Novikov

Protoshchak

et al. 2021

Vestn. rentgenol. radiol.

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The true causes of sexual disorders after radiation treatment of prostate cancer, among which the central role is occupied by erectile dysfunction, are still not fully clarified. The number of patients who undergo various radiation-exposure options as a radical therapy is steadily increasing, which makes the issue very relevant. This literature review provides up-to-date data on the most studied probable mechanisms of the erectile function status decline after radiation therapy for prostate cancer.

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“…К тому моменту был проведен ряд дозиметрических исследований, результаты которых показали отсутствие корреляции величины лучевой нагрузки на область СНП при БТ с частотой РИЭД [30]. Эта связь до сих пор не подтверждена ни одним клиническим рандомизированным исследованием, в то время как за последние 5 лет опубликован ряд экспериментальных данных, указывающих на существенную роль радиационной нейропатии в патогенезе РИЭД [8,31,32]. Несмотря на эти противоречия, с учетом абсолютно очевидной главенствующей роли повреждения СНП при РПЭ как причины послеоперационной ЭД наряду с усовершенствованием систем планирования ЛТ проводятся исследования по разработке методик нервосберегающей ЛТ РПЖ [33].…”

Section: сосудосохраняющаяunclassified

Radiation-induced erectile dysfunction in patients with prostate cancer: current methods of radiotherapy

Novikov¹,

Новиков²,

Protoshchak³

et al. 2020

Onkourologiâ

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In recent years, significant changes have taken place in the treatment of prostate cancer. Modern radiation treatment technologies are beginning to take a leading position not only in localized and locally-advanced forms of the disease, but also in the case of oligometastatic process. This encourages a natural interest in various aspects of radiation therapy of prostate cancer, in particular its effects on erectile function status. Analysis of domestic literature shows the complete absence of publications on the technical possibilities of radiation therapy to preserve potency after treatment. The purpose of this work was to highlight this critical issue.

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Cavernous Nerve Injury by Radiation Therapy May Potentiate Erectile Dysfunction in Rats

Cited by 23 publications

References 29 publications

Chronic administration of LIMK2 inhibitors alleviates cavernosal veno-occlusive dysfunction through suppression of cavernosal fibrosis in a rat model of erectile dysfunction after cavernosal nerve injury

Chronic administration of LIMK2 inhibitors alleviates cavernosal veno-occlusive dysfunction through suppression of cavernosal fibrosis in a rat model of erectile dysfunction after cavernosal nerve injury

Radiation-Induced Erectile Dysfunction in Prostate Cancer Patients: Up-to-Date View on Pathogenesis

Radiation-induced erectile dysfunction in patients with prostate cancer: current methods of radiotherapy

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