Abstract
Erectile dysfunction (ED) is a significant cause of reduced quality of life in men and their partners. Cavernous nerve injury (CNI) during pelvic surgery results in ED in greater than 50% of patients, regardless of additional patient factors. ED related to CNI is difficult to treat and typically poorly responsive to first- and second-line therapeutic options. Recently, a significant amount of research has been devoted to exploring neuroprotective and neuroregenerative approaches to salvage erectile function in patients with CNI. In addition, therapeutic options such as neuregulins, immunophilin ligands, gene therapy, stem cell therapy and novel surgical strategies, have shown benefit in pre-clinical, and limited clinical studies. In the era of personalized medicine, these new therapeutic technologies will be the future of ED treatment and are described in this review.
Highlights
Erectile dysfunction (ED) is the recurrent and persistent inability to achieve and maintain an erection adequate to permit sexual performance for at least 3 months [1]
phosphodiesterase type 5 inhibitors (PDE5i) have been the mainstay treatment of ED for years
Studies have proven efficacy of these medications in certain populations, patients with Cavernous nerve injury (CNI) after pelvic surgery, or multiple medical comorbidities are more complex, rendering these medications less effective [128]. These difficult-to-treat patient populations have a poor quality of life (QOL) related to relationship and sexual dissatisfaction
Summary
Erectile dysfunction (ED) is the recurrent and persistent inability to achieve and maintain an erection adequate to permit sexual performance for at least 3 months [1]. The European Male Ageing Study (EMAS) reported a prevalence of 30–64% and approximately one-third of men in their population were dissatisfied with their overall sexual relationship [5]. The CNs originate from the pelvic ganglia (PG) and contain both sympathetic and parasympathetic nerve fibers. These nerves are almost exclusively unmyelinated and release the neurotransmitters for penile innervation [10,11]. OTfhtihs einPnKovRa-tlivkee fiennddionpglaosffmerisc arenteiwcumluemchkainniasmse (PERK) / activating transcription factor 4 (ATF4) signaling pathway [32]. This innovative finding offers a new mechanism for a local upsurge in a neurotrophin that has already demonstrated. The results of early work investigating BDNF in CNI models are promising, but further work in the field is required to optimize the clinical administration and utilization of this neurotrophin
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