madman
Super Moderator
Erectile dysfunction (ED) is a common disorder—about 50% of males between the ages of 40 and 70 are affected.1Currently, there is (at least via public perception) a notion that ED treatments for mild to moderate ED have been very successful. Treatment for most men is based on pharmacotherapy with phosphodiesterase (PDE) type 5 inhibitors;2 however, besides pharmacotherapy, the treatment of ED has been managed by numerous approaches, including, for example, vacuum constriction, intracorporal injection therapy, intraurethral alprostadil, penile implants, revascularization, platelet-rich plasma, and stem cell therapy.3,4 Although many patients with ED experience high efficacy with PDE type 5 inhibitors, this therapy is inadequate in approximately 30-40% of patients, and particularly in some specific groups such as diabetic men.5 In addition, PDE inhibitors can result in adverse effects; moreover, some patients may not be eligible for this therapy, for example, patients receiving nitrates who are at risk of developing hypotension. Thus, there is still a significant unmet medical need for the development of more effective therapeutic strategies for the treatment of ED.
Nonetheless, in the end, the application of gene therapy for ED represents an exciting opportunity to push the field forward—as suggested by the recent spate of published reviews.3,4,8-10 In fact, gene therapy for ED may provide the best therapeutic option for patients with, for example, severe cardiovascular disease, nitrate prescriptions, diabetes, obesity, and those who have undergone radical prostatectomy. Moreover, gene therapy for ED has 4 major intrinsic advantages: (i) the penis is easily accessible and the desired gene can be administered directly into the corporal tissue, without entering the systemic circulation; (ii) corporal vascular smooth muscle cells of the penis have a relatively low turnover rate, thus allowing the desired gene to be expressed for long periods of time; (iii) the vascular smooth muscle cells of the penis are interconnected by gap junctions permitting relatively low transfection efficiency due to the resulting syncytial smooth muscle cell network; and (iv) transduced genes to the penis may affect any aspect of the erectile process by selectively altering the expression of a given molecular target, and thus, target disease-specific gene products that may improve the erectile response.11
CONCLUSION
There is still very scarce public/general recognition of the unmet medical need for improved ED treatment of the growing clinical population. However, gene therapy for ED is not dead but remains a hopeful and novel therapeutic area for the treatment of ED. This may be particularly applicable to patients who respond poorly to PDE5 inhibitors.
Nonetheless, in the end, the application of gene therapy for ED represents an exciting opportunity to push the field forward—as suggested by the recent spate of published reviews.3,4,8-10 In fact, gene therapy for ED may provide the best therapeutic option for patients with, for example, severe cardiovascular disease, nitrate prescriptions, diabetes, obesity, and those who have undergone radical prostatectomy. Moreover, gene therapy for ED has 4 major intrinsic advantages: (i) the penis is easily accessible and the desired gene can be administered directly into the corporal tissue, without entering the systemic circulation; (ii) corporal vascular smooth muscle cells of the penis have a relatively low turnover rate, thus allowing the desired gene to be expressed for long periods of time; (iii) the vascular smooth muscle cells of the penis are interconnected by gap junctions permitting relatively low transfection efficiency due to the resulting syncytial smooth muscle cell network; and (iv) transduced genes to the penis may affect any aspect of the erectile process by selectively altering the expression of a given molecular target, and thus, target disease-specific gene products that may improve the erectile response.11
CONCLUSION
There is still very scarce public/general recognition of the unmet medical need for improved ED treatment of the growing clinical population. However, gene therapy for ED is not dead but remains a hopeful and novel therapeutic area for the treatment of ED. This may be particularly applicable to patients who respond poorly to PDE5 inhibitors.
Last edited:
