Neuroprotective and Nerve Regenerative Approaches for Treatment of Erectile Dysfunction after Cavernous Nerve Injury

Campbell, Jeffrey; Burnett, Arthur L.

doi:10.3390/ijms18081794

Cited by 39 publications

(24 citation statements)

References 128 publications

(161 reference statements)

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“…Cavernous injury, diabetes, and other types of ED-associated disorders are not significant for first-line clinical treatment with PDE5i, so more treatment regimens and means are needed for Ed treatment [25]. At present, the relationship between RhoA/ROCK signaling and ED has attracted the attention of many researchers.…”

Section: Discussionmentioning

confidence: 99%

Effect of HongJing I in Treating Erectile Function and Regulating RhoA Pathway in a Rat Model of Bilateral Cavernous Nerve Injury

Zhao

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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HongJing I (HJI), a traditional Chinese herbal formula, has been confirmed to be effective for the clinical treatment of erectile dysfunction (ED). However, the mechanism of action of HJI remains unclear. Here, we aimed to investigate the effect and underlying mechanisms of HJI against ED in a rat model of bilateral cavernous nerve injury (BCNI). Rats were divided into five groups: normal control (NC), BCNI-induced ED model (M), M + low-dose HJI (HL), M + medium-dose HJI (HM), and M + high-dose HJI (HH). All groups were treated with normal saline or the relevant drug for 28 consecutive days after inducing BCNI-ED. At the end of the treatment period, the intracavernous pressure (ICP) was recorded, and histological examination was conducted using Masson’s trichrome staining. Immunofluorescence staining and western blotting were applied to detect the changes in fibrosis protein and Ras homolog A (RhoA), Rho-associated protein kinase 1 (ROCK1), and ROCK2 expression. We found that HJI effectively improved the ICP in the treatment groups. In addition, RhoA, ROCK1, and ROCK2 expression levels were increased upon BCNI-ED induction, and HJI successfully inhibited cavernosum fibrosis and the activation of RhoA/ROCK2 signaling. Overall, these results suggest that the effects of HJI in attenuating ED may be caused, at least in part, by the suppression of RhoA/ROCK2 signaling and alleviation of fibrosis. However, the precise mechanism surrounding this requires further investigation in future studies.

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Section: Discussionmentioning

confidence: 99%

Effect of HongJing I in Treating Erectile Function and Regulating RhoA Pathway in a Rat Model of Bilateral Cavernous Nerve Injury

Zhao

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…As it pertains to ED, PRP has been found to contain growth factors such as vascular endothelial growth factor (VEGF), plateletderived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor (IGF), and fibroblast growth factor (FGF) (18,19). Many of these growth factors have been shown to have a role in improving erectile function in both preclinical and clinical studies (20). Specifically, animal studies injected with VEGF and using a cavernous nerve injury (CNI) model of ED have shown greater salvage of erectile function compared to controls (21).…”

Section: Platelet-rich Plasma (Prp)mentioning

confidence: 99%

“…There is a lack of understanding as to whether PRP can play a neuroprotective or nerve regeneration role in salvaging erectile function after CNI, and additional studies comparing early versus delayed administration would be beneficial (20). Currently, the Mayo Clinic (Rochester, MN, USA) is recruiting patients for a clinical trial that involves the application of autologous PRP circumferentially around the neurovascular bundle during a radical prostatectomy as a neuroprotective mechanism (https://clinicaltrials.gov/ct2/ show/NCT02957149) (12).…”

Section: Platelet-rich Plasma (Prp)mentioning

confidence: 99%

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The good, bad, and the ugly of regenerative therapies for erectile dysfunction

Campbell¹,

Milenković²,

Usta³

et al. 2020

Transl Androl Urol

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Erectile dysfunction (ED) is a common condition which reduces quality of life of both patients and their partners, and is a significant health care expense every year. Although phosphodiesterase type-5 inhibitors are the current first-line treatment for men with ED, they are limited by their on-demand dosing, intolerance, and variable efficacy in complex patient populations such as men with multiple medical comorbidities or ED after pelvic surgery. Regenerative medicine has been introduced and investigated in andrology as an encouraging strategy to restore diseased erectile tissue structure and function. Novel regenerative therapies for ED are controversial but are perceived to offer a durable and safe tissue restorative approach to act as a long-term solution to this cumbersome disease process. Here, we review platelet-rich plasma, amniotic fluid membranes, low-intensity extracorporeal shockwave therapy, and stem cell therapy as regenerative strategies to treat ED. Most of these approaches have preclinical and occasionally clinical data to support their ongoing investigation; however, none of these treatments are currently supported for use in ED patients outside of clinical trials.

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“…Prostate cancer is the second leading cause of cancer-related death in men worldwide [1, 2]. Erectile dysfunction (ED) administered by injury of cavernous nerve is a significant problem following prostate cancer surgery, which seriously affects the quality of life of patients [3–5]. Adipose tissue-derived stem cells (ADSCs) has significant treatment effect for ED in diabetics, post-prostatectomy patients, and those with peyronie’s disease [6, 7].…”

Section: Introductionmentioning

confidence: 99%

IcarisideII facilitates the differentiation of ADSCs to SCs via let-7i/STAT3 axis to preserve erectile function

Guo

Shen

2019

Biol Res

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Background IcarisideII (ICAII) could promote the differentiation of adipose tissue-derived stem cells (ADSCs) to Schwann cells (SCs), leading to improvement of erectile function (EF) and providing a realistic therapeutic option for the treatment of erectile dysfunction (ED). However, the underlying molecular mechanisms of ADSCs and ICAII in this process remain largely unclear. Methods ADSCs were treated with different concentrations of ICAII. Cell proliferation was determined by MTT assay. qRT-PCR and western blot were performed to detect expressions of SCs markers, signal transducer and activator of transcription-3 (STAT3), and microRNA-let-7i (let-7i). Luciferase reporter assay was conducted to verify the regulatory relationship between let-7i and STAT3. The detection of intracavernosal pressure (ICP) and the ratio of ICP/mean arterial pressure (MAP) were used to evaluate the EF in bilateral cavernous nerve injury (BCNI) rat models. Results ICAII promoted cell proliferation of ADSCs in a dose-dependent manner. The mRNA and protein levels of SCs markers were increased by ICAII treatment in a dose-dependent manner in ADSCs. Moreover, let-7i was significantly decreased in ICAII-treated ADSCs and upregulation of let-7i attenuated ICAII-induced promotion of SCs markers. In addition, STAT3 was a direct target of let-7i and upregulated in ICAII-treated ADSCs. Interestingly, overexpression of STAT3 abated the let-7i-mediated inhibition effect on differentiation of ADSCs to SCs and rescued the ICAII-mediated promotion effect on it. Besides, combination treatment of ADSCs and ICAII preserved the EF of BCNI rat models, which was undermined by let-7i overexpression. Conclusion ICAII was effective for preserving EF by promoting the differentiation of ADSCs to SCs via modulating let-7i/STAT3 pathway.

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Neuroprotective and Nerve Regenerative Approaches for Treatment of Erectile Dysfunction after Cavernous Nerve Injury

Cited by 39 publications

References 128 publications

Effect of HongJing I in Treating Erectile Function and Regulating RhoA Pathway in a Rat Model of Bilateral Cavernous Nerve Injury

Effect of HongJing I in Treating Erectile Function and Regulating RhoA Pathway in a Rat Model of Bilateral Cavernous Nerve Injury

The good, bad, and the ugly of regenerative therapies for erectile dysfunction

IcarisideII facilitates the differentiation of ADSCs to SCs via let-7i/STAT3 axis to preserve erectile function

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